Adenovirus-mediated overexpression of GR (subtype β) resulted, apart from the development of hepatic steatosis, in the increase in tumor-necrosis factor-α (TNF-α) and activation of its downstream signaling, nuclear factor-kappaB (NF-kB), in HFD-treated mice [52]. The gene discussed is NR3C1; the disease is Hepatic steatosis.