Shi et al. (40) reported that in ApoE−/− mice, plaque size was observed after treatment with recombinant (r)IL-22 and IL-22 mAb, which revealed that Th22 cell-derived IL-22 activated IL-6/STAT3, increased dendritic cell-induced Th17-cell proliferation, stimulated SMC dedifferentiation to a synthetic phenotype, and ultimately promoted the development of atherosclerosis. The gene discussed is STAT3; the disease is atherosclerosis.