A series of immune checkpoints (e.g., PD-1 [1], adenosine [2]), metabolism dysregulation in the tumor microenvironment (TME) (e.g., amino acid metabolism [3], lipid metabolism [4]), immunosuppressive cells (e.g., regulatory T cells (Tregs) [5], tumor-associated macrophages (TAMs) [6]) and immunosuppressive cytokines (e.g., TGF-β, IL-6, IL-10), could cause the dysfunction of these immune cells by exhaustion, or phenotype differentiation. Here, IL10 is linked to neoplasm.