The strongest genetic risk factor for SpA in humans is the human major histocompatibility complex (MHC) class I allele HLA‐B27, which is believed to contribute to arthritis by promoting intestinal dysbiosis by driving endoplasmic reticulum stress and activation of the unfolded protein response upon HLA‐B27 misfolding, and by activating CD8+ cytotoxic T cells upon recognition of arthritogenic peptides (Dumas et al, 2020; Kavadichanda et al, 2021). This evidence concerns the gene CD8A and arthritic joint disease.