They likely complement conventional adaptive αβ T cell immunity, by permitting pathogen-specific responses to microenvironmental niches with compromised MHC expression, either resulting from viral immune evasion (for CMV and EBV), infection of cells devoid of MHC (e.g., red blood cells in the case of P. falciparum), or conceivably class I MHC loss during tumor development and immune evasion. Here, HLA-C is linked to neoplasm.