Whereas interference with the mouse homologue of ERAP1 has been shown to drastically alter tumor recognition by both T and NK cells [50], ERAP2 has no known mouse homologue, is less tightly coordinated with MHC-I [51], [52]in vitro and in vivo, and is believed to have a more specialized role than ERAP1, i.e. ERAP2 only trims a limited subset of peptide antigens. The gene discussed is ERAP2; the disease is neoplasm.