Specifically for hematopoiesis and hematological malignancy, knocking out p16 and p14 in mice has been shown to increase HSC self-renewal and repress differentiation, while also promoting cancer (38, , –41); however, the impact of p15 loss is unclear as when deleted in mice, p15 does not significantly increase cancer development without additional perturbations and p15 knockout promotes HSCs differentiation (42, –44). The gene discussed is CDKN2B; the disease is hematologic disorder.