Weathington confirmed that IL-22, the main effect molecule of Th22 cell, can bind to the IL-22RA receptor, activating JAKI–STAT1 and STAT3 pathways, regulating Akt, ERK, JNK and p38 signal, thus participating in the regulation of renal fibrosis [26]. The gene discussed is AKT1; the disease is renal fibrosis.