AML blasts induce a senescent phenotype in the stromal cells within the bone marrow microenvironment, driven by p16INK4a expression; in turn, the p16INK4a-expressing senescent stromal cells promote blast AML survival and proliferation, a phenomenon mediated through AML-induced NOX2-derived superoxide [192]. The gene discussed is CYBB; the disease is acute myeloid leukemia.