AML tumors in the context of TSC present bi-allelic inactivating mutations in TSC1 or TSC2. These genes encode the proteins hamartin and tuberin responsible for the inhibition of the mammalian target of rapamycin (mTOR), a conserved protein kinase that regulates cell growth and metabolism in response to growth factors and nutrients [9]. The gene discussed is TSC2; the disease is acute myeloid leukemia.