In addition, KLF5 also interacted with the RAR, and synthetic RAR ligands modulated KLF5 transcriptional activity and affected stress responses in the cardiovascular system in a KLF5‐dependent manner.24 Consistently, ATRA inhibited the proliferation of intestinal epithelial cells by inhibiting the expression of KLF5.25 Synthetic retinoid Am80 suppresses KLF5 expression and smooth muscle phenotypic modulation and in‐stent neointima formation.26 Thus, the induction of TNFAIP2 by RA may be cell line‐specific and KLF5‐independent. This evidence concerns the gene KLF5 and rheumatoid arthritis.