In NAFLD patients, hepatic activities of HSD11B1 decrease, whereas the cortisol-inactivation enzyme increase [22, 154], which may result in local GC deficiency and concomitant activation of the hypothalamic–pituitary–adrenal (HPA) axis to trigger GC release [22, 154]. This evidence concerns the gene HSD11B1 and metabolic dysfunction-associated steatotic liver disease.