Genetically, mutations in thymidine kinase genes (TK2) [4] and ribonucleotide reductase regulatory TP53 inducible subunit M2B (RRM2B) [5] are responsible for myopathic form of MDS, while mutations of SUCLA2 (succinate-CoA ligase ADP-forming beta subunit) [6] and SUCLG1(succinate-CoA ligase alpha subunit) [7] are related to encephalomyopathic form of MDS. Here, TK2 is linked to myelodysplastic syndrome.