In 2010, Hidvegi et al. demonstrated that the FDA-approved drug and autophagic inducer named CBZ enhanced autophagic (independently of mTOR) and proteasomal degradation of Z-AAT, leading to reduction of the intrahepatic PAS + D inclusions, liver fibrosis, and inflammation in an AATD mouse model [72]. This evidence concerns the gene MTOR and alpha 1-antitrypsin deficiency.