The antiapoptotic members of the Bcl-2 family (Bcl-2 and Bcl-XL) showed inhibited expression during the development of NAFLD, while the level of proapoptotic members (Bak1 and Bax) was upregulated (Figures 3(c)–3(f)). This evidence concerns the gene BAK1 and metabolic dysfunction-associated steatotic liver disease.