SERPINI1 and hereditary angioedema: These can exhibit a loss-of-function phenotype due to a deficiency in the levels of active serpin, such as found in hereditary angioedema caused by deficiency of the C1 inhibitor [5], and/or a toxic gain-of-function phenotype due to the deposition of serpin long-chain oligomers (polymers) in tissue, as in the case of familial encephalopathy with neuroserpin inclusion bodies (FENIB; caused by the polymerisation of neuroserpin) [6,7].