Beyond modulating the immune microenvironment through 4-1BB agonism or CSF-1R inhibition, TGF-β in particular has shown to be a primary mechanism of tumor immune evasion by blocking the TH-1 effector phenotype, inhibit T cell division/function and natural killer (NK) cell function, and by promoting epithelial-mesenchymal transition (EMT) (34, 35). This evidence concerns the gene CSF1R and neoplasm.