Acute myeloid leukemia (AML) blasts induced a senescence-associated secretory phenotype (SASP) in BM stromal cells through a p16INK4a-dependent mechanism, which encompassed the irreversible arrest of cell proliferation and the secretion of a set of chemokines, proinflammatory cytokines, and growth factors (Abdul-Aziz et al., 2019). The gene discussed is CDKN2A; the disease is acute myeloid leukemia.