As they are tumor suppressor genes, mutation of TSC1 or TSC2 leads to loss of inhibitory influence on the cell cycle by hyperactivation of the mTOR protein (mammalian target of rapamycin), culminating in disordered proliferation of tissues and formation of hamartomas—benign tumor-like lesions—in several tissues, in addition to other manifestations such as neurodevelopmental disorders and epilepsy.1, 2, 3, 4. Here, MTOR is linked to neoplasm.