M-CSF, through binding to its receptor CSF-1R, not only activates signaling pathways such as PI3K/Akt and MAPK, driving TAM survival and proliferation, but also induces TAM polarization towards the immunosuppressive M2-like macrophages, reinforcing their supportive role in promoting tumor cell growth (18, 21, 67). Here, AKT1 is linked to neoplasm.