Researchers have attempted to elucidate the pathological mechanisms of NASH-HCC using several genetically modified mouse models [8], such as farnesoid X receptor knockout mice [9], melanocortin 4 receptor (Mc4r) knockout mice [10] and transmembrane 6 superfamily member 2 (TM6SF2) knockout mice and rats [11–13] as well as non-genetically modified animal models that receive mutagenic reagents (e.g., streptozotocin) [14] and undergo dietary modification. The gene discussed is TM6SF2; the disease is metabolic dysfunction-associated steatohepatitis.