We further demonstrated that the autoantigenic ADAMTSL5 epitope is generated through NH2-terminal trimming of precursor peptides by the endoplasmic reticulum aminopeptidase 1 (ERAP1) [38], clarifying the functional consequences of the gene–gene interaction between HLA-C*06:02 and ERAP1 variants in psoriasis susceptibility [39]. The gene discussed is ERAP1; the disease is psoriasis.