By activating CB2 on tumor-associated macrophages (TAMs), the phenotype can flip from a tumor-supportive M2-like state to an M1-like anti-tumor state while simultaneously promoting recruitment and activation of cytotoxic T cells and inhibiting the release of pro-tumor cytokines like IL-10 and transforming growth factor-beta (TGF-β). Here, TGFB1 is linked to neoplasm.