On the other hand, if our idea is correct that the dominant inhibitory effect of Mfn2 400Q relates to its disruption of both homotypic (i.e. Mfn2-Mfn2) and heterotypic (i.e. Mfn1-Mfn2) mitofusin interactions, then its pathological potential should be equally great in mammalian heart disease. Here, MFN2 is linked to heart disorder.