Evidence from cells lacking endogenous GR (e.g., U2OS/COS7 cells), transformed cells (e.g., rat hepatoma cells or leukemia cell lines), or yeast systems showed that GR activation is maximal when the relative phosphorylation of GR at Ser211 surpasses that of Ser226 [10,12,23,35]. Here, NR3C1 is linked to hepatocellular carcinoma.