These data suggest that the MTA1-dependent activation of the mTOR/S6K/4EBP1/CyclinD1 pathway may represent a mechanism through which prostate cancer progresses under conditions of PTEN loss, which suggests a direct positive crosstalk between the MTA1 and mTOR pathway independent of the MTA1/PTEN link [11]. The gene discussed is MTOR; the disease is prostate carcinoma.