Although PiZ transgenic mice are extensively used as a model of AATD‐associated liver disease, differences to the human situation have to be taken into account: Due to multiple insertion of the transgene in PiZ mice, higher amounts of aggregates are found compared to humans [27] who display large interindividual variations in their hepatic AAT content [4]. This evidence concerns the gene SERPINA1 and alpha 1-antitrypsin deficiency.