In an in vivo model of cisplatin-induced AKI, UCA1 is upregulated and promotes inflammation by sponging miR-4498 to derepress AKT3; knockdown of UCA1 reduces circulating cytokines and lowers tubular epithelial apoptosis in a T-cell/TEC co-culture system, supporting an immunomodulatory role of the UCA1–miR-4498–AKT3 axis in AKI [75]. Here, AKT3 is linked to acute kidney injury.