Besides Th17 cells and ILC3s, we also found that IL-17-producing γδ T cells preferentially expressed Tmem176a and b. In fact, the development of psoriasis-like dermatitis in which these cells are central was partially reduced in Tmem176b single-deficient mice, suggesting an important intrinsic role of both homologues in these emerging players of type 17 immunity. This evidence concerns the gene TMEM176B and psoriasis.