Consistent with reports linking DGCR8 activity to stem cell self-renewal and malignant transformation [9,10] and its association with stemness, DNA damage tolerance, and drug resistance phenotypes [20], its progressive upregulation in higher-risk MDS may reflect an adaptive mechanism aimed at sustaining minimal miRNA processing capacity under oncogenic stress, thereby supporting the persistence of undifferentiated progenitor cells. This evidence concerns the gene DGCR8 and myelodysplastic syndrome.