Consistent with our findings, previous studies have shown that upregulation of Wnt/β-catenin signaling can exert protective effects in disease models such as diabetic nephropathy, where pharmacological activation of suppressed Wnt proteins—such as Wnt1, Wnt4, and Wnt5a—was associated with reduced cellular damage and fibrosis [54]. This evidence concerns the gene WNT4 and diabetic kidney disease.