Thus, in the TSC lesions confined to the CNS, mTOR hyper-activation leads to a direct reprogramming of the self-renewal and differentiation capacity of the cells endogenous to the tissue in which the lesions are found, while the etiology of mTOR hyper-activation to the appearance of LAM-associated lesions in the lung, kidneys, and uterus is much less clear. The gene discussed is MTOR; the disease is lymphangioleiomyomatosis.