Intriguingly, a MYC-dependent expression of HDAC2 enzyme can be induced upon loss of the APC tumor suppressor in colorectal tumorigenesis, while crossing of HDAC2 mutant with tumor-prone APCmin mice is able to produce significantly lower, as compared to APCmin mice (with unimpaired HDAC2), tumor rates [134,151,161], strongly indicating the prominent contribution of specific mutational signatures and tumor settings to the modulation of HDAC2 oncogenic, or onco-repressive function. Here, HDAC2 is linked to neoplasm.