 I'd like to begin by thanking Anagha and Sanjeev for inviting me to this wonderful conference and for the warm hospitality shown to me. With that, let's now switch gears and apply some of the insight that we gained in the morning lectures. Take you on a journey along some unusual liver lesions, which you won't see very often, but if you work in a tertiary care center, you're likely to see them once in a while. We know that a wide gamut of lesions affects the liver and we've heard from Dushyan the accuracy of CT and of course added MR in the case of liver has improved our accuracy both for the purpose of detection and characterization of liver lesions. It's always important to see the background liver because that changes our differential in the context of interpretation of focal liver lesions. So this talk is going to be more of a pattern approach to seeing lesions that are not so commonly encountered in liver imaging. I won't go through this long list of lesions, but for the purpose of this talk we'll try and focus on the less common entities. So let's begin by seeing this incidentally discovered lesion in a 25-year-old lady. On ultrasound we just saw this very mildly hypoechoic lesion, barely perceptible and on the T2-rated MR images you can barely identify this lesion, but you know on ultrasound there was a lesion and once you inject contrast you can see that there is subtle enhancement which becomes more prominent in the venous phase and this is the one-hour delayed phase. This we've used gadolinium-bopter which is the only liver specific contrastation that we have available in our country. So on that one-hour delayed hepatocyte phase you can see that this lesion is brighter than the background liver. Now there are very few lesions which do that and the hallmark of this finding is of course focal nodular hyperplasia which shows this very homogeneous increased uptake because remember FNH is not a true tumor, it's a hamartometous lesion comprised of normal hepatocytes. They express the OATP receptors and therefore they take up this liver specific contrast agent and they have poorly developed biliary canaliculi so they're not able to excrete that contrast into the bile channels and therefore this lesion appears hyper intense as compared to the background liver. The other lesions which can do this are well differentiated HCC but then it tends to be more patchy and heterogeneous rather than this kind of a homogeneous uptake of gadolinium-bopter on the hepatocyte phase and some of the liver cell adenomas can also show this finding. This 32-year-old lady with pain in the right upper quadrant, this is an in an opposed phase sequence which incidentally is a very important sequence in liver imaging and must always be a part of your routine protocol. So you can see here there is a lesion behind the right hepatic vein and on the opposed phase image this shows a very marked signal drop. It's mildly hyper intense on the T2 weighted image and when you inject contrast there is evidence of arterial enhancement which shows washout in the venous phase and in the hepatocyte phase it is hyper intense as compared to the background liver. Now the key finding here is this marked signal drop on the opposed phase image which suggests that there is intravoxel fat. Increasingly we don't talk of intracellular fat but intravoxel fat and that is seen in liver cell adenomas so this lesion with this set of findings is a liver cell adenoma. This is again a rare lesion we don't see that often. We know it's commonly seen in women in the reproductive age group who are on oral contraceptives. If there are more than 10 lesions in the liver it's referred to as adenomatosis. It's also seen in the background of patients with glycogen storage diseases and patients who are on anabolic steroids. Occasionally you'll see this in the pediatric age group in patients who have tyrosinemia. So the hallmark of course again just to reiterate is the loss of signal on the opposed phase image arterial enhancement which may or may not persist in the venous phase. There is a new genetics based classification of liver cell adenomas. Initially in 2016 they divided into four types pathologists love to add on entities to their complex classifications. We now have six different types of adenomas on pathology. You have the inflammatory adenoma which is the one which is more prone to hemorrhage and we know that hemorrhage is one of the hallmarks of liver adenomas which on CT will be seen as a hyper density and on MR will be seen as a T1 hyper intensity. It is the HNF1-alpha mutated type of adenoma which shows this diffuse intralesional fat. So if we were to further sub- classify the lesion which I just showed you that it would best fit at the HNF1-alpha mutated type of adenoma. Then there are beta-catenin-activated adenomas which could be mutated in exon-3 or exon-7 not much of imaging differentiation between these two and then there is a sonic hedgehog type and an unclassified type. The important entities to remember are the inflammatory adenomas which are more prone to developing hemorrhage and the HNF1-alpha mutated type of adenoma which shows this intralesional fat and therefore signal drop on the opposed phase image. This is again a rare kind of an appearance where you have multiple adenomas look at the very dramatic signal drop that you get on the opposed phase image in this patient who was who had liver cell adenomatosis. When you see echogenic lesions on ultrasound in a routine day you think of hemangiomas but look at other findings as well. There is no distal enhancement. In fact there is some manifestation of a speed propagation artifact. There is a step in the contour of the diaphragm and this is a fat-containing lesion which on CT shows you the typical fat value. So this is a lipoma or a fat predominant angioma lipoma. Both of them can look very similar. This is a different patient who had tuberous cirrhosis. Look at the AML in the kidney and you have this fat-containing lesion in the liver. Incidentally I'll talk of this again towards the later part of the talk. These lesions are now classified as picomas. They are better referred to as picomas and that's the term that should be used. If you see the liver studded with equal-sized less than a centimeter lesions which are very bright on T2 which do not communicate with the biliary tree which show just mild peripheral enhancement or no enhancement then you're dealing with the entity of biliary hematomas. It is a manifestation of a ductile plate anomaly. No communication with the biliary tree. In fact in this patient we had an argument with our gastroenterology colleagues because this patient was jaundiced. Notice the dilated biliary tree. There's a calculus at the lower end and the liver is studded with these T2 bright lesions which are less than a centimeter in size and almost all of them are of the same size and the gastroenterologists argued that these should be collangular abscesses but this is definitely not collangular abscess. You will never have 100 collangular abscesses in the liver. All of them equal size evenly distributed throughout the liver. This is a diagnosis that only you can make. These are biliary hematomas or the one-man bugs complex. No touch lesions. Nothing needs to be done. This is a very unusual case that I would like to share with you. This was a 40-year-old BSF Javan who came from JNK and he was carrying multiple CTs and MRs done over a period of four to five years which were showing this lesion in the right lobe of the liver which was almost remaining stable. No definite increase in size showed this kind of peripheral calcification as well as some amorphous kind of calcification in the center of the lesion. We were really not sure what we were dealing with. We did an MR and on the MR we could see that this lesion is essentially not uniformly T2 bright but there are T2 dark areas. Only a very small area was showing diffusion restriction and it showed heterogeneous peripheral kind of enhancement. There was some dilatation of the biliary tree which we thought was because of the location of the lesion. On T2 weighted images there was this kind of a micro-visicular appearance. There were multiple tiny cysts which were seen in the background of this larger single lesion. We really did not know what this was but when we looked at the literature when you see a lesion which looks like a tumor remains stable over five to six years shows these kind of tiny cysts on MR which are not perceptible on CT. Think of this entity of echinococcus multi-locularis. This is not the common garden variety of hydated that we see in India that is echinococcus granulosis. This form is in fact more common in Europe and the findings that have been highlighted in the literature are presence of both central and peripheral calcification. Remember the common garden variety of hydated does not show central calcification that's almost a rule. You only get peripheral capsular calcification in a echinococcus granulosis. Then the lesion looks and mimics a tumor because it has an exogenous kind of proliferative growth and if you look at a T2 weighted image and you can identify these micro vesicles very tiny cysts studying the entire lesion. Remember to think of this entity and of course the final proof would come on histology. If you have a lesion which has fluid attenuation small areas of fat some calcification we know that whenever derivatives of all three germ layers are present anywhere you've got to think of a teratoma and liver is no exception you can get occasionally you can get teratomas in the liver as well. We need to learn from our mistakes as Dushyant was also talking about because we're not going to live long enough to make all of them ourselves.