However, compelling transgenic mouse model studies have established that Jak2 is essential for hematopoietic stem and progenitor cell functions [58, 59], and that conditionally deleting Jak2 in the MPLW515L-mutant MPN clone profoundly modifies myelofibrosis-like disease, including allelic burden, which has not been achieved to this extent with first-generation JAK inhibitors [30]. Here, JAK2 is linked to myeloproliferative neoplasm.