Reports indicate that in mutant mice with sustained cell surface expression of the TNFRSF1A receptor, this constitutive TNFR1 signaling exacerbates the pro-inflammatory and pro-fibrotic features of non-alcoholic steatohepatopathy but is not linked to the appearance of hepatic steatosis (39). The gene discussed is TNFRSF1A; the disease is Hepatic steatosis.