CDKN2B and acute myeloid leukemia: As the release of NICD depends on the cleavage of Notch1 by γ‐secretase.[20] We blocked the cleavage by RO4929097,[21] an inhibitor of γ‐secretase which inhibited the expression of p15 in KG1a and HL60 cells with ANXA1 knockdown (Figure 4D), thereby promoting the proliferation of AML cells (Figure 4E), showing that the transcription activation of p15 depended on the nuclear translocation of NICD.