Since the discovery of the involvement of deregulated tyrosine kinases in the pathophysiology of these diseases, and particularly the identification of the fusion gene FIP1L1-PDGFRA, new molecules inhibiting specifically this signaling pathway (imatinib) were individualized, leading to dramatic therapeutic benefits in proliferative forms of HES considered before that of very poor prognosis.     ///    [Durable efficacity and remission after treatment with imatinib mesylate for FIP1L1-PDGFRA transcript negative associated eosinophilic cardiomyopathy].. 