Cancer-derived extracellular vesicles increase M2 polarization by activating signaling pathways such as STAT3, p38MAPK, NF-κB, ERK1/2, and PI3K/AKT [28,29,30] and reprogram M1 tending cells into the cancer-promoting M2 end of the macrophage phenotype spectrum. Here, AKT1 is linked to cancer.