We discovered that several of the genes capable of reversing mitochondrial fragmentation in OPA1 mutant cells with the most severely fragmented mitochondrial network (Fig 2D) also led to hypertubulation in control fibroblasts (Fig 2F), including known components of the mitochondrial fission apparatus (DNM1L, MIEF1, MFF, SLC25A46), which demonstrates in patient fibroblasts that imbalanced mitochondrial dynamics can be genetically re‐equilibrated, as previously documented in animal models of MD (Chen et al,2015; Wai et al,2015; Yamada et al,2018). This evidence concerns the gene DNM1L and Menkes disease.