IGF1R and neoplasm: (93) to clarify the mechanisms underlying the onset and proliferation of TC demonstrated that release of IGF-1 by M2-like tumor-associated macrophages promoted metastasis and increased the stemness of ATC cells via insulin receptor-A/IGF1R-mediated activation of the phosphoinositide 3-kinase (PI3K)/alpha serine/threonine-protein kinase (AKT)/mammalian target of rapamycin (mTOR) signaling pathway (93).