For example, simultaneous interrogation of clonal and non‐clonal populations in individuals with BCR‐ABL‐negative MPNs, as well as chronic myeloid leukaemia (CML), showed significant enrichment of inflammatory pathways including IL‐6, transforming growth factor beta (TGFβ) and TNFα‐associated signalling in wild‐type HSCs in patients with CML9 and in patients with JAK2V617F+ myelofibrosis,10 in comparison to HSCs in age‐matched, healthy donors. The gene discussed is TGFB1; the disease is myelofibrosis.