Induction of RORγt under Th17 cell-polarizing conditions is dependent upon STAT3, which perceives and transduces signals from IL-6, IL-23 and other cytokines (29) and IL-6 can upregulate IL-21 expression through the STAT3 pathway, which in turn increases IL-23 receptor and RORγt expression, and the combination of RORγt and STAT3 further promotes IL-17 expression (31), which also inhibits forkhead transcription factor p3 (FOXP3) expression (32), thereby promoting the development of atherosclerosis. This evidence concerns the gene STAT3 and atherosclerosis.