Therapeutically, CD47 blockade enhances the efficacy of EGFR‐targeted treatments, and CD47 expression in GBM correlates with both EGFR and c‐Src activity, highlighting a cooperative immune evasion mechanism through the EGFR–c‐Src–TRIM21–CD47 axis [5]. The gene discussed is EGFR; the disease is glioblastoma.