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]. Here, TSC1 is linked to acute myeloid leukemia.