Alternative genetic models to study NASH progression and (spontaneously developing) HCC are the Tsumura-Suzuki Obese Diabetes (TSOD) mice, keratin 18-, NF-κB essential modulator (NEMO)-, and methionine adenosyltransferase 1A (MAT1a)-deficient models [92]. This evidence concerns the gene KRT18 and metabolic dysfunction-associated steatohepatitis.