The inability of mitochondria to adequately supply ATP, leading to energy depletion, is central to the loss of contractile function in pathological cardiac hypertrophy and heart failure.[16] It is well established that ECSIT copurifies with OXPHOS assembly chaperones.[9] Our data show that ECSIT‐X4 is predominantly localized in the mitochondria of adult hearts (Figure 1F). This evidence concerns the gene ECSIT and heart failure.