Cardiac LC amyloidosis also altered mitochondrial function in cardiac fibroblasts exposed to patient-derived pre-amyloidogenic LC (Imperlini et al., 2017) through the interaction of the amyloidogenic LC with the mitochondrial protein VDAC1 and optic atrophy protein 1 (OPA1) (Lavatelli et al., 2015). Here, OPA1 is linked to laryngotracheoesophageal cleft.