While other environmental exposures like obesity and alcohol use could additionally contribute to the liver dysfunction in these patients (these risk factors have been previously implicated [15, 45–47]), the interaction between dysfunctional SERPINA1 alleles and hepatitis C leads to the hypothesis that the mechanism by which the exposure of hepatitis C infection interacts with the underlying genetic risk of AATD is through parallel mechanisms of hepatocyte injury via endoplasmic reticulum dysfunction [41, 50]. The gene discussed is SERPINA1; the disease is hepatitis C virus infection.