As some small-molecule JAK2 inhibitors have shown efficacy in murine models of MPL W515L [20, 21], identification and characterisation of further cases of non-familial, MPL S505N-mutated MPN is required as these patients may benefit therapeutically from such strategies and also to determine features that may influence the risk of both thrombotic events and fibrotic disease progression. The gene discussed is MPL; the disease is myeloproliferative disorder.