JAK-2 inhibitor therapy, currently considered to be the mainstay-of-treatment for myelofibrosis, can be effective in reducing splenic volume and minimise disease-related symptoms (thus improving the quality of life) even in patients with CALR-positive post-ET myelofibrosis [33]; however, these agents have no effect on the underlying clonal proliferation, nor can they change the course of the disease. The gene discussed is CALR; the disease is myelofibrosis.