Malignant cells escape immunosurveillance by different mechanisms, some of which are: (1) reduced immune recognition (including loss of tumor antigen expression and MHC class I and costimulatory molecule expression), (2) increased resistance to apoptosis (through STAT3 signaling), or (3) development of an immunosuppressive tumor microenvironment (including the production of cytokines, e.g., VEGF, TGF-β, IL-10 and increased expression of immunoregulatory molecules, e.g., PD-1/PD-L1, TIM-3, LAG-3), which lead to the development of malignant diseases (48, 50). Here, TGFB1 is linked to neoplasm.