[15] Loss of Slc25a51 gene in cardiomyocytes induces cardiac hypertrophy by impairing complex I respiration and mitochondrial NAD+ level.[16] Slc25a49 (Mtch1) is a penta‐spanning transmembrane protein situated in the outer mitochondrial membrane.[17] Our recent study revealed that SLC25A49 deficiency disrupted OXPHOS and energy production, signifying its crucial function in cellular energy metabolism,[18] with a metabolic abnormal phenotype similar to Dox‐induced cardiac mitochondrial damage. Here, MTCH1 is linked to cardiac hypertrophy.