However, STAT activation is a feature of several experimental models of kidney disease and is thought to contribute to renal fibrosis and disease progression, (Bienaime et al., 2016; Chuang & He, 2010; Dai et al., 2013; Zheng et al., 2019) therefore, it is unlikely that its activation by CT‐1 accounts for the beneficial effect observed in our study. The gene discussed is SOAT1; the disease is renal fibrosis.