Similarly, in humans, childhood-onset mitochondrial disease and exercise intolerance have been observed for both dominant [54] and recessive mutations [55] in SLC25A4. Given the implication that mitochondrial functional deficits might underlie the negative lactation effects highlighted in the current study, it would be intriguing to examine the phenotypes of homozygous cows further in this context. This evidence concerns the gene SLC25A4 and inborn mitochondrial metabolism disorder.