GSK-J4, an inhibitor KDM6 proteins, to the BM LSKs from each mouse cohort and performed methylcellulose medium supported colony formation assays. Significantly reduced colony formation was observed in both the double lesion and TET2 deficiency groups (p<0.01 and p<0.05)....KDM6B-TET2 double lesion model demonstrate that KDM6B overexpression and TET2 deficiency cooperatively cause significant hematopoietic impacts and drive development of myeloid disorders mediated by profound dysregulation of innate immune and genomic stability regulatory signaling in BM HSPCs.