HLA-C and neoplasm: Tumor-infiltrating T cells can either receive a “natural” activation signal 1 through a T cell receptor (TCR) due to its interaction with peptide–MHC complexes (endogenous immunity) or receive one “artificially” by a T cell bispecific antibody (TCB) simultaneously bound to a tumor cell surface antigen and the CD3e chain of the TCR complex leading to redirected T cell-mediated tumor cell killing (synthetic immunity) [2,5,6,7,8,9].