Given that complete knockout (KO) of MFN2 is embryonic lethal in mice and loss of function mutations in humans lead to the severe mitochondrial disease Charcot Marie Tooth Type 2A (CMT2A) [92], the heterozygous carriers of this variant as detected in centenarians may minimally reduce protein abundance or function. This evidence concerns the gene MFN2 and inborn mitochondrial metabolism disorder.