The exact mechanisms include: (1) tumor neoantigen presentation, structure, and processing are genetically or epigenetically altered, which, thus, influences the activation of immune response and recruitment of effector T cells [7]; (2) alterations in the structure of MHC II/I due to gene defects affect antigen presentation and, ultimately, immune response [38]; (3) dysfunctional interferon (INF) signaling pathway causes inadequate anti-tumor T cell effector function [43,44]. This evidence concerns the gene CBLIF and neoplasm.