Possible mechanisms of resistance to BETis encompass AMPK-ULK1-mediated autophagy in AML [76,77], NF-κB in colorectal cancer [78], PP2A phosphatase and BCL2L1/BCL-X in breast cancer [79], the GLI2-dependent Hedgehog pathway in pancreatic cancer [80] and kinome reprogramming in ovarian cancer [81], among others. The gene discussed is BCL2L1; the disease is acute myeloid leukemia.