Despite the plethora of genetic and molecular specificities that may underlie LNCaP cells' response to this or any other therapeutic scheme, the consistency observed for both early and advanced ETV1‐overexpressing cell models (PNT2‐ETV1 and LNCaP cells, respectively) regarding activation of EGFR and STAT3, as well as their effective response to the corresponding inhibitors Erlotinib and TTI‐101, respectively, sustains the potential of combining these inhibitors to efficiently target prostate carcinomas with ETV1 overexpression. The gene discussed is ETV1; the disease is prostate carcinoma.