CDKN2A and acute myeloid leukemia: indicated that the BSJ-mediated degradation can protect the CDK6-p16(INK4A)/p18(INK4C) complexes and that INK4 levels define the proliferative response to the degradation of CDK6, which reveals that INK4 proteins can be used as predictive signals for CDK6-targeted therapy in acute myeloid leukaemia.25