However, recent work revealed that key molecules of necroptosis—the programmed form of necrosis—mediated by receptor interacting protein kinase (RIPK) 1, RIPK3 and mixed lineage kinase domain-like pseudokinase (MLKL)—are major contributors in the pathophysiology of NASH, fibrosis and liver cancer development (21–23). The gene discussed is RIPK3; the disease is metabolic dysfunction-associated steatohepatitis.