Retinoic acid (RA) has been extensively characterised as a key mediator in promoting the expression of α4β7 and CCR9 and the development of a gut homing phenotype in CD4+ T cells.31,32 However, it is striking that while RA acts as a protolerogenic factor in terms of its effects on T cell polarisation, it acts opposingly to IL-36 stimulation in this regard.32 Indeed, stimulation with IL-36 is sufficient to overcome the protolerogenic effects of RA on CD4+ Th cells, while further enhancing the expression of α4β7 (Supplementary fig. 6). The gene discussed is CD4; the disease is rheumatoid arthritis.