TP53 and metabolic dysfunction-associated steatotic liver disease: However, certain events have been observed: the proliferation of oval cells, which are progenitors of hepatocytes implicated as the origin of many liver tumors, including in patients with NAFLD 22; increased production of reactive oxygen species and oxidative injury 23,24; and mutations in regulatory genes, including tumor suppressors such as p53 and phosphatase tensin homolog (PTEN) 25.