Concurrently, the PI3K/AKT nexus integrates metabolic-proliferative cascades across pathologies: HDAC5 activates PI3K/AKT for fibrotic transformation in diabetic kidney disease, FTO stabilizes RUNX1 mRNA to activate PI3K/AKT-mediated fibrosis in obstructive nephropathy, and WTAP-mediated S1PR3 stabilization stimulates tumor proliferation in renal cell carcinoma (Wang et al., 2024a). This evidence concerns the gene AKT1 and renal cell carcinoma.