As transmission electron microscopy (TEM) has been used to examine ultrastructural changes in mitochondria that are relevant to AD pathogenesis [21,58,59], future studies should consider the use of TEM to conduct a more detailed examination of mitochondrial morphological changes that result from depletion of Willin/FRMD6, particularly since the present study suggests that decreased Willin/FRMD6 affects processing of mitochondrial inner membrane protein OPA1 and thus may potentially affect the organization of the mitochondrial cristae. The gene discussed is IMMT; the disease is Alzheimer disease.