AKT and mTORC1 are activated downstream of RTKs and promote endocrine therapy resistance.14–16 We reported PRCP maintains levels of activated AKT (S473 phosphorylated) in pancreatic cancer cells.13 Therefore, we hypothesized PRCP may promote endocrine therapy resistance by regulating RTK signaling, including activation of AKT. The gene discussed is PRCP; the disease is pancreatic neoplasm.