Drosophila models of CMT2-associated mutations in Mitofusin2 (MFN2), have revealed that both loss- and gain-of-function human variants of MFN2 cause CMT-associated neurodegeneration and have implicated excessive mitochondrial fusion and disrupted mitochondria-ER contacts in disease pathogenesis (El Fissi et al., 2018; Shen et al., 2021). Here, MFN2 is linked to Charcot-Marie-Tooth disease.