When IGF-1R is activated, which means phosphorylation occurs, it affects tumor physiological activities through multiple downstream pathways, in this study, IGF-1R regulates NPC cell proliferation in bone through the AKT/mTORC1/S6 signaling axis, it is worth noting that the site where AKT undergoes phosphorylation is Ser473, rather than Thr308, and the site where S6 undergoes phosphorylation is Ser235/236, rather than Ser240/244. This evidence concerns the gene IGF1R and neoplasm.