Although the clinical use of EGFR TKIs is essentially restricted to EGFR‐mutated NSCLC, our data imply that selected contexts of clinical resistance to MET‐TKIs may represent a prime example of beneficial targeting of wt EGFR. We duly caution that further work on a larger scale is needed to validate our model of deregulated miR‐205‐ERRFI1‐EGFR axis in MET‐addicted tumors. The gene discussed is MET; the disease is non-small cell lung carcinoma.