Examples of the involvement of canonical IGF-1R activity include the observation that specific inhibitors targeting the MAPK and PI3K pathways reduced IGF-1-induced invasion ability of prostate cancer cells (362), or that IGF-1, primarily functioning through the PI3K/AKT/mTORC1 pathway, promotes the growth of preneoplastic prostate epithelial cells by counteracting autocrine TGF-β suppression of Survivin transcription (363). This evidence concerns the gene IGF1R and prostate cancer.