The observed higher levels of circulating VEGF in patients undergoing long-lasting treatment with the pan-tyrosine kinase inhibitor dasatinib, together with the paradoxical development of reversible PAH in this subset population, point to the RTK remodeling process triggered by chronic VEGF ligand engagement with VEGFR2, which contributes to RTK upregulation and the subsequent hyperproliferative, apoptosis-resistant cellular phenotype, as a liable mechanism of angiogenesis resistance in this pathophysiological context [3,4,50]. The gene discussed is KDR; the disease is pulmonary arterial hypertension.