Additionally, considering a recent study reporting activating mutations in ETV1 as possible drivers of NSCLC progression and resistance to anti‐EGFR therapy [47], it is also likely that the relevance of the identified ETV1‐EGFR/STAT3 signaling axis may extend beyond prostate carcinomas, namely, to other carcinomas frequently exhibiting overexpression of ETV1 (e.g., gastrointestinal stromal tumors and melanomas) [48]. The gene discussed is STAT3; the disease is carcinoma.