Moreover, considering that not only mitochondrial respiration defects but also growth retardation are commonly observed in Shmt2-knockout MEFs14 and in SHMT2-knockout human cell lines15–17, growth retardation alongside mitochondrial respiration defects in the foetal livers of Shmt2-knockout embryos would also be involved in the manifestation of anaemia. This evidence concerns the gene SHMT2 and anemia.