An increase of double-strand breaks (DSB) was observed in MDS, together with an impaired DDR, due to an altered pattern of phosphorylated DDR key proteins, including TP53. A reduced expression of TP53 after phosphorylation presumably indicated impaired downstream signaling of DNA damage and/or defects in downstream components of the DDR [36]. This evidence concerns the gene TP53 and myelodysplastic syndrome.