In a series of 31 CALR mutated IFN-treated patients with ET, Verger and colleagues performed targeted sequencing and found six of 31 patients having one or more additional mutations in ASXL1, IDH1/2, TET2, or TP53. Strikingly, patients with no additional mutations had a significantly better response to IFN compared to patients presenting with ≥1 of those mutations suggesting ASXL1, IDH1/2, TET2 or TP53 may be associated with resistance to treatment [75]. Here, CALR is linked to essential thrombocythemia.