 The study found that acute depletion of TBP in mice does not affect the overall activity of Paul II, but rather impairs the initiation of INA polymerase III. The authors suggest that this TBP-independent transcription mechanism may be due to the formation of the TFIID complex, which is able to function even without TBP or TRF2. Despite having reduced levels of TAF4 and TFIIA, the Paul II machinery remains intact and is capable of supporting TBP-independent transcription. This article was authored by Jane Z. J. Kwan, Thomas F. Nguyen, Anil I. C. Yuzozi and others.