Most authors evaluate the disease as a spondyloarthropathy (MHC-I-opathy) based on Human Leukocyte Antigen (HLA) class I association and epistatic endoplasmic reticulum aminopeptidase 1 (ERAP-1) interactions, increased T helper (Th) 17 type immune response, neutrophilic inflammation and barrier dysfunction in environmentally exposed organs (5). This evidence concerns the gene ERAP1 and spondyloarthropathy.