METTL14 and renal fibrosis: Conversely, other studies reported that METTL14 overexpression in HG-treated HK-2 cells led to inactivation of the PI3K/Akt signaling pathway and down-regulation of HDAC5, which are closely associated with epithelial–mesenchymal transition (EMT) in renal tubular cells during DN progression (94) EMT of renal tubular epithelial cells is a key driver of renal fibrosis in DN, and the PI3K/Akt pathway is widely involved in this process (95–97).