Therefore, it is very likely that the doses of JAK2 inhibitors employed, that are constrained by development of dose-dependent thrombocytopaenia and anaemia reflecting the essential role of JAK2 in normal haematopoiesis, are not sufficiently high to abrogate JAK2 signalling to such an extent to induce clonal cell death. This evidence concerns the gene JAK2 and anemia (phenotype).