Ross et al. (2019) have recently reported that deletion of TFAP2A (the gene encoding AP-2α) significantly attenuates the TGF-β induced maturation of myofibroblasts although the underlying mechanism is unclear. Traditionally, transcription factors are notorious to target in drug development. Recent successes in “drugging” such transcription factors as p53 (Khoo et al., 2014) and c-Myc (Dang et al., 2017) may shed some light on this issue should further evidence present AP-2α and/or KLF15 as a desirable target in the intervention of renal fibrosis. This evidence concerns the gene TFAP2A and renal fibrosis.