Such liver pathology is specifically associated with genotypes leading to the abnormal polymerization of AAT within the hepatocytes’ endoplasmic reticulum, notably the PI*ZZ phenotype of AATD, caused by homozygous NM_000295.5:c.1096G>A p.(Glu366Lys) substitution [38]. This evidence concerns the gene SERPINA1 and alpha 1-antitrypsin deficiency.