Cover: Confocal microscopy analysis of autophagosome LC3B (red) and mitochondrial marker TOMM20 (green) shows that the mitophagosomes formation is not impaired in CMT2A^MFN2 cells. Mitophagy has been assessed upon CCCP induction. Despite the few autophagosomes, most of them are engaged in engulfing mitochondria in CMT2A^MFN2 fibroblasts, as shown by LC3B/TOMM20 colocalization signals regardless of the treatment conditions. AKT-mTOR pathway representation shows that decreased autophagy and increased proliferation are both regulated by AKT activation in CMT2A^MFN2 fibroblasts. AKT full activation requires phosphorylation of Thr(308) by PDK1 and Ser(473) by mTORC2, to activate cellular proliferation; inhibit autophagy; promote mitochondrial fission. mTORC2 kinase activity is suppressed by the interaction with MFN2. Miransertib (yellow), a specific AKT inhibitor, enables restoration of the decreased autophagy and increased cell proliferation.