The occurrence of optic atrophy in the context of pathogenic MFN2, WFS1 and CISD2 mutations provides strong supportive evidence that RGC survival is detrimentally affected as a result of impaired interactions between the mitochondrial network and the endoplasmic reticulum, especially if there is disturbed calcium flux between these compartments [28]. The gene discussed is MFN2; the disease is Leber hereditary optic neuropathy.