Specifically, the broad spectrum of RTK inhibition targeted by dasatinib and the blockade of specific RTK like ephrin receptor kinases—which are actively involved in VEGF–VEGFR2 endocytosis and endosomal-dependent degradation—seem to partially explain the pathogenic role of dasatinib in the development of PAH and the divergent therapeutic outcomes compared to other VEGFR antagonists [113,114,115] (Figure 3). This evidence concerns the gene VEGFA and pulmonary arterial hypertension.