ECSIT is required for stabilization of complex I assembly[17b] and its absence results in impaired complex I assembly, accumulation of intermediates, and subsequently mitochondrial dysfunction.[8, 9, 10] Moreover, ECSIT deficiency leads to decreased levels of many mitochondrial subunits,[9] and this mirrors the phenotype of NDUFA13 deficient cells.[30] Notably, the mutation ratio of the Ecsit gene allele is not high in patients with CRC (Figure S17C, Supporting Information), and this may reflect that loss‐of‐function mutation of Ecsit is incompatible with life. This evidence concerns the gene NDUFA13 and colorectal carcinoma.