Given the implication of the inflammatory cytokine IL-23 in the pathogenesis of autoimmune and inflammatory diseases, such as inflammatory bowel disease, psoriasis, psoriatic arthritis, and multiple sclerosis (Teng et al., 2015), it is imperative to investigate how the development and function of IL-23–producing cDCs can be modulated under pathogenic conditions. This evidence concerns the gene IL23A and psoriatic arthritis.