While AMPK appeared important at early stages of the apoptotic response induced by venetoclax, increased AMPK activity was detected in tissue samples from chronic lymphocytic leukemia patients relapsing from venetoclax therapy compared to pretreatment samples, suggesting that a deregulation of the metabo-energetic machinery occurred in cells escaping Bcl-2 inhibition [23]. This evidence concerns the gene PRKAA1 and B-cell chronic lymphocytic leukemia.