Based on the mechanisms of resistance observed in other cancers in which these drugs are used, e.g., non-small cell lung cancer (NSCLC) and head and neck cancer [32,33,34], the therapeutic failure observed in CRPC patients has been generally assumed to be due to the functional redundancy of EGFR/ERBB, MET and IGF-1R, which activate largely overlapping signaling pathways including Ras-Raf-MAPK and PI3K/AKT/mTOR pathways [72,84]. This evidence concerns the gene MTOR and cancer.