Specifically, blunted imiquimod-induced dermatitis in GPR15L-deficient mice, or the GPR15L peptide injection-induced dermatitis, could in part be explained by the known role of GPR15L in the GPR15L–GPR15 axis and subsequent recruitment of dendritic epidermal T-cells (5, 6, 26), or in keratinocyte proliferation (27). This evidence concerns the gene GPR15LG and dermatitis.