Very recently, Shi et al. (2020) found that lncRNA H19 levels were increased in a time-dependent manner in human dermal microvascular endothelial cells with TGF-β2 treatment and renal tissue of STZ-induced CD1 mice, and that gene knockdown of H19 in diabetic mice partially restored renal function along with mitigated renal fibrosis, and increased expression of CD31 but decreased expression of FSP-1 in renal tissues of these gene-modified diabetic mice through inhibiting TGF-β/SMAD3 signaling transduction (Shi et al., 2020). The gene discussed is TGFB1; the disease is renal fibrosis.