In the last decade, cytogenetics and DNA sequencing have allowed for investigating the molecular alterations found in HES, demonstrating that somatic mutations are usually uncommon in patients harboring PDGFRα, PDGFRβ, or PCM1-JAK2 rearrangements, but significantly more frequent in FGFR1 rearranged cases [24]. The gene discussed is PDGFRA; the disease is hypereosinophilic syndrome.