Downregulation of p16INK4a using siRNA targeting CDKN2A increased cell division during clonal expansion58 and neural stem cell self‐renewal depended on repression of CDKN2A. 59Taken together, we postulated that CDKN2A is a good candidate of therapeutic target to control BM microenvironment because early senescence is reversible through de‐induction of CDKN2A. 60However, a larger study using BM‐MSCs derived from a more homogeneous population of patients is needed in order to clarify the contribution of CDKN2A and other markers in the premature senescence of BM‐MSCs in MDS and MM. This evidence concerns the gene CDKN2A and myelodysplastic syndrome.