Another Tk2 targeted mouse carrying an amino acid substitution (Tk2H126N) found in a pediatric patient with MDS may represent a better model for this disease; similar to the Tk2−/− mouse, it displays complete postnatal lethality and mitochondrial defects, but there are also clear manifestations of neurological malfunction including tremors, weakness, decreased activity and altered gait [74]. This evidence concerns the gene TK2 and myelodysplastic syndrome.