Together, we propose a model for co-treatment-induced signaling mechanism for macrophage alternative activation: co-treatment induces arginase-1 expression through PPARγ and HIF-2α, leading to macrophage alternative activation, and simultaneously it activates Akt1/mTOR to promote survival and growth of the alternatively activated macrophages in the tumor microenvironment. This evidence concerns the gene AKT1 and neoplasm.