We turned to glioblastoma multiform (GBM)-associated mutations in the extracellular domain of EGFR (R84K and A265V point mutations), which were recently shown to drive an ~650-fold increase in the dimerization affinity of EREG- and EPGN-bound receptors with only a 6-fold change to ligand-receptor binding (Hu et al., 2022). The gene discussed is EREG; the disease is glioblastoma.