Although initially identified as a lipid kinase, AGK has been shown to phosphorylate GSK3β at Ser9 and PTEN at Ser380, Thr382, and Thr383 residues to inactivate them, leading to enhanced PI3K-AKT activation in renal cell carcinoma cells (RCC) and CD8+ T cells respectively 23, 26. This evidence concerns the gene CD8A and renal cell carcinoma.