Previous data showed that in Tsc1−/− and Tsc2−/− cells, loss of Tsc1/Tsc2 activated mTOR and down-regulated PDGFR expression; inhibition of mTOR by rapamycin restored PDGFR expression and subsequently enhanced phosphatidylinosital 3-kinase (PI3K)/AKT activation, which reversed the impaired tumor formation by Tsc1−/− and Tsc2−/− cell lines [13], [14]. Here, AKT1 is linked to neoplasm.