 Chronic diabetes leads to many serious complications. One of the most common and debilitating is diabetic retinopathy, an eye disorder that is characterized by damage to the vessels that supply oxygen and nutrients to the retina, the light detecting part of the eye. Although diabetes-induced changes in blood glucose levels are known to damage retinal blood vessels, how blood vessel repair processes are affected by diabetes remains largely unknown. This study found that the protein Ataxia telangiectasia mutated, or ATM, is critical for retinal blood vessel repair and that ATM is improperly regulated in patients with diabetic retinopathy. In bone marrow, hematopoietic stem cells, or HSCs, divide for self-renewal and help in the repair of damaged blood vessels. This means that the HSC population must remain active to keep generating new cells that can be used to repair damaged blood vessels. However, diabetes causes surges in glucose levels that lead to DNA damage in HSCs, resulting in loss of this unique population. In cells, ATM helps correct DNA damage by recruiting DNA repair proteins to sites of DNA damage. The authors of this report hypothesized that during diabetes, ATM is needed for the survival of long-term repopulating HSCs in bone marrow and that the loss of ATM leads to inflammation in retinal blood vessels and, eventually, the development of diabetic retinopathy. To determine the importance of ATM in bone marrow cells and their role in retinal blood vessel repair, the researchers replaced the bone marrow of normal mice with bone marrow from mice lacking the ATM gene. When these mice were treated with a drug that induces diabetes, their bone marrow had a smaller number of long-term repopulating HSCs. In addition, their retinas contained more non-functional blood vessels and a higher level of inflammation, both of which are features of diabetic retinopathy. These results showed that diabetic retinopathy occurred in diabetic mice when ATM was absent from HSCs. To confirm the importance of ATM for preventing diabetic retinopathy in humans, the investigators compared gene expression patterns between chronic diabetes patients with and without diabetic retinopathy. In line with the function of ATM in diabetic mice, patients with diabetic retinopathy had lower expressions of ATM and other genes involved in the cell cycle and DNA repair. These findings provide the first evidence that ATM is critical for preventing diabetic retinopathy because this protein maintains an appropriate HSC population in bone marrow and enables retinal blood vessel repair. Future studies could search for additional factors that promote HSC survival or enhance bone marrow function as a treatment for diabetic retinopathy.