Since multiple RTK pathways are activated in PCa by SEMA3C, it is not surprising that targeting single RTKs individually would be ineffective due to redundancy of bypass RTK pathways and could explain intrinsic resistance of PCa to targeted RTK therapies such as EGFR inhibitors (erlotinib, gefitinib) as well as anti-HER2-targeted antibody therapeutics (pertuzumab, trastuzumab) [92,93]. This evidence concerns the gene EGFR and posterior cortical atrophy.