Our recent work confirmed that PC-1/PrLZ interacts with 4E-BP1, a downstream factor of mTOR, and mains its protein stability via blocking ubiquitin-mediated proteasome degradation, through which PC-1/PrLZ inhibits autophagy and contributes to chemoresistance of prostate cancer cells [14]. The gene discussed is MTOR; the disease is prostate carcinoma.