The inhibitors against PI3K/mTOR pathway sensitize chronic myeloid leukemia stem cells with tyrosine kinases like nilotinib as well as restore the response of progenitors against nilotinib even in the presence of stem cell factor.140 On the other hand, pharmacological inhibition of mTOR was reported with increased expression of CD133 in gastric cancer both in time and dose-dependent fashion.141 Yang and colleagues have revealed that suppression of mTOR signaling markedly blocked the conversion of CD133+ to CD133− in liver cancer. The gene discussed is PROM1; the disease is liver cancer.