It has been demonstrated that single-cell multi-omics of DNMT3A p.R882 CD34+ HSC populations in MM patients revealed a myeloid-biased differentiation and megakaryocytic expansion within humans, suggesting that broad transcriptional consequences of DNMT3A mutation affect differentiation, even in the absence of a strong exogenous source of inflammation [45]. The gene discussed is DNMT3A; the disease is Miyoshi myopathy.