PI3K/Akt in TAMs integrates CSF1R/IGF-1R/TLR inputs to drive mTORC1-linked biosynthesis and secretion of IL-6, TGF-β, and pro-angiogenic factors, which in turn activate survival/DNA-repair pathways in adjacent tumor cells and generate leaky neovasculature that impairs drug delivery. This evidence concerns the gene IGF1R and neoplasm.