In essence, there is an ongoing “yin-yang” between (a) frameshift mutations in tumor cells leading to T cell (Fig. 6, purple) recognition of tumor; (b) upregulation of PD-L1 on tumor cells as a consequence of T cell recognition; (c) loss of T cell recognition of peptide-MHC complexes due to β2M mutations; and (d) potential activation of components of the innate immune system (natural killer (NK) cells). The gene discussed is B2M; the disease is neoplasm.