As IM inhibits PDGFR and c-Kit, two other transmembrane TKs, it has been approved as frontline therapy for: (i) gastrointestinal stromal tumors (GIST), characterized by mutated and over-expressed c-Kit or PDGFR-b [5]; (ii) other myeloid malignancies and hypereosinophilic syndromes and (iii) systemic mastocytosis [6,7]. The gene discussed is PDGFRB; the disease is hypereosinophilic syndrome.