However, an experimental in vivo mouse model involving site-directed mutagenesis (to replace AAT M351 with valine (V) and M358 with leucine (L)) revealed maintenance of antiprotease activity under oxidant stress despite abrogation of wild-type AAT function, indicating a potential novel strategy for treatment of AATD [112]. This evidence concerns the gene SERPINA1 and alpha 1-antitrypsin deficiency.