In diabetic nephropathy studies show that GAS5 is reduced in renal tissue and in high-glucose-challenged tubular cells, and that restoring GAS5 attenuates oxidative stress, pyroptosis, and profibrotic signaling through miRNA axes such as GAS5/miR-452-5p and GAS5/miR-221 [91,92]. Here, GAS5 is linked to diabetic kidney disease.