This lineage bias is particularly pronounced in MDS-STAG2-mutant clones, which drives the malignant expansion of granulosa–monocyte progenitors and the transformation of these cells to AML by destabilizing the E-P loop in the CTCF deletion region and down-regulating transcriptionally pausing genes (e.g., RUNX1 targets) [61–63]. The gene discussed is STAG2; the disease is acute myeloid leukemia.