OPA1 and autosomal dominant optic atrophy: Cells derived from patients with ADOA, including lymphoid cells and fibroblasts, demonstrate consistently reduced mitochondrial function, with variably abnormal mitochondrial morphology and increased susceptibility to apoptosis.6,12,13,27 Augmentation of OPA1 in patient cells, as shown by others using AAV expression,28 CRISPR-Cas9-directed OPA1 mutation repair25 or by STK-002 as shown in this work, can improve parameters of mitochondrial respiratory function.