In addition, the ENO1‐Y189E mutant plasmid, in which the Y189 site was mutated to glutamicacid (E), was constructed to mimick the phosphorylated‐Y189 form of ENO1.[47, 48] Notably, the expression of ENO1‐Y189E restored the binding of ENO1 to GRB2 and SOS1, which was reversed by stably knocking down GRB2 and transfecting PCa cells with a GRB2mut plasmid (Figure 5N; Figure S4I, Supporting Information). This evidence concerns the gene SOS1 and posterior cortical atrophy.