SERPINA1 and alpha 1-antitrypsin deficiency: To develop iPSC-based model systems of disease, we first prepared a bank of >60 iPSC clones (ten clones per donor; partial set and reprogramming methodology described previously [Mills et al., 2013; Somers et al., 2010]) derived from the dermal fibroblasts of three control individuals without any known disease and three recruited volunteers previously diagnosed with AATD due to homozygous inheritance of mutant Z alleles encoding the AAT protease inhibitor (PiZZ genotype, a common monogenic cause of hepatic cirrhosis [Eriksson et al., 1986]).