NR4A1 and neoplasm: Thus, persistently elevated or relatively invariant levels of cortisol may, in turn, stimulate tumor proliferation via differential gluconeogenesis in normal and tumor tissues, activation of hormone receptors in the tumor, or immunosuppression (Sapolsky and Donnelly, 1985; Ben-Eliyahu et al., 1991; Sephton and Spiegel, 2003; Asher and Sassone-Corsi, 2015; Longo and Panda, 2016).