Previous data showed that inhibition of mTOR by rapamycin up-regulated PDGFR expression in Tsc1−/− and Tsc2−/− cells, and subsequently enhanced PI3K/AKT activation, which reversed the impaired tumor formation by Tsc1−/− and Tsc2−/− cell lines [13], [14]. The gene discussed is AKT1; the disease is neoplasm.