In our study, we detected the upregulation of other transcription factors that contribute to Th17 differentiation, such as BATF, which remodels chromatin to enable the access of transcription factors to Th17-specific loci53; Hif-1α, which can directly increase RORγt expression and drive IL-17A expression with RORγt54; and IL-23A, which is essential for the induction of pathogenic Th17 cells55 in the skin of Nfkbiz−/− mice with dermatitis (Fig. S3). Here, HIF1A is linked to skin disorder.