We took advantage of the favorable properties of AMC11–siRNA formulations to knock down p42-MAPK and/or Rheb proteins in LNCaP and PC3 cells in order to explore whether reducing the levels of proteins involved in tumoral cell proliferation and survival signaling pathways could boost the anticancer effects of DTX, a drug commonly used in prostate cancer treatment. The gene discussed is RHEB; the disease is prostate carcinoma.