It is now well known that first- (imatinib) and second- (dasatinib, nilotinib) generation TKIs act on different molecular targets [14], and that their side effects are mainly due to the inhibition not only of BCR-ABL1 but also of other tyrosine kinases such as c-kit, PDGFR, Src or EPHB4. Imatinib mainly causes peripheral edema, whereas dasatinib predisposes some patients to pleural effusions and, to a lesser extent, pulmonary arterial hypertension [15], and inhibits platelet function [16, 17]. Here, BCR is linked to pulmonary arterial hypertension.