Regarding cancer progression and senescence, co-cultures of human primary AML with human BM derived-MSC with knockdown of the p16 gene reduced AML cell proliferation; moreover, co-culture of AML cells with non-silenced MSC for 6 days reduced lamin B1 expression, increased IL-6 and IL-8 production and the frequency of MSC positive for senescence-associated β-galactosidase (SA-β-Gal) staining, and induced MSC expression of p16 and p21 [42], showing that LSC can also influence the microenvironment to induce senescence compatible features that, eventually, foster their own expansion. The gene discussed is CDKN1A; the disease is acute myeloid leukemia.