The first evidence linking BLVRB redox activity to hematopoietic cell fate originated from a large-scale genetic screen of cohorts with thrombocytosis (high platelet counts) [21], in which a redox-defective mutation (BLVRBS111L) was genetically associated with both clonal and non-clonal disorders of thrombocytosis. Here, BLVRB is linked to thrombocytosis disease.