Our demonstration that miR‐205‐driven ERRFI1 loss is sufficient to confer vicarious oncogenic properties to EGFR signaling is congruent with (i) biochemical studies that assign to ERRFI1 a role as pan‐ERBB inhibitor; (ii) genetic analyses in the mouse that have nominated Errfi1 as a tumor suppressor; (iii) biological experiments in glioblastoma, NSCLC, and pancreatic carcinoma cells that point to ERRFI1 loss as key mechanism in sustaining oncogenic addiction to EGFR signaling (reviewed in Anastasi et al, 2016). This evidence concerns the gene ERRFI1 and glioblastoma.