Additionally, the SH2 domain involves the binding of GRB2 to receptor proteins, thereby recruiting GRB2 and SOS1 to the membrane and mediating signal transduction.[35] We stably knocking down GRB2 with transfecting PCa cells with a GRB2 mutant plasmid deficient in bases expressing the SH2 domain sequence (GRB2mut), and found that activation of the MAPK signaling pathway was abolished (Figure 4I). This evidence concerns the gene GRB2 and posterior cortical atrophy.