No human genomic mutations leading to total MTIF3 deficiency have been reported, but the studies outlined above suggest that MTIF3 may influence obesity predisposition and weight loss potential by modulating mitochondrial function; thus, MTIF3 may play a key role in adipose tissue metabolic homeostasis, as adipocyte mitochondria not only provide ATP, but also impact adipocyte-specific biological processes such as adipogenesis, lipid metabolism, thermogenesis, and regulation of whole-body energy homeostasis (Gregoire et al., 1998; Boudina and Graham, 2014). Here, MTIF3 is linked to obesity disorder.