We subsequently asked whether a pro-inflammatory milieu, in the presence or not of an autocrine loop sustained by CCL2 itself, could induce CCR2 expression in a driver-mutated hematopoietic clone (CD34+ cells from one CALR type-II-mutated ET, one JAK2V617F-mutated PV and one CALR type-I-mutated ET) and in the JAK2V617F-mutated cell line HEL. This evidence concerns the gene CALR and essential thrombocythemia.