A tumor organoid originating from a mouse or human tissue or after oncogenic transformation can maintain genetic and phenotypic characteristics of its progenitor; accordingly, the Akt inhibitor MK-2206 and the mechanistic target of rapamycin (mTOR) inhibitor ridaforolimus have been proven to be significantly effective against organoid formation; these findings are consistent with the already-known AR and PI(3)K signaling activation in prostate cancer (Chua et al., 2014). The gene discussed is MTOR; the disease is prostate cancer.