SLC25A4 and inborn mitochondrial metabolism disorder: A long-standing mystery in the mitochondrial disease field is how dominant mutations in SLC25A4 (encoding adenine nucleotide translocase 1 [Ant1]) cause such a wide spectrum of clinical and molecular phenotypes that are not observed in patients with homozygous null SLC25A4 (Kaukonen et al., 2000; Siciliano et al., 2003; Simoncini et al., 2017; Palmieri et al., 2005; Napoli et al., 2001; Deschauer et al., 2005; Thompson et al., 2016; Echaniz-Laguna et al., 2012; Tosserams et al., 2018; Kashiki et al., 2022).