This was further recapitulated by pathway analysis whereby INFγ and INFα response gene sets, as well as the JAK–STAT signaling pathway, showed strongly enriched activity (Extended Data Fig. 7d), providing additional support for our hypothesis that the pre-LSCs represent residual persister cells of the preceding MPN or CMML disease rather than healthy hematopoietic stem or progenitor cells (HSPCs). This evidence concerns the gene SOAT1 and myeloproliferative disorder.