[40,54,55] Although in most cases, only one of these two pathologic mechanisms may contribute to the development of HE, there are patients in whom neoplastic eosinophils have been described to produce autocrine eosinophil growth factors (IL-3, IL-5) themselves Furthermore, overproduction of HE-promoting cytokines may stem from another (noneosinophilic) clonal process such as a T-cell lymphoma or the L-HES [4,37]. This evidence concerns the gene IL5 and hereditary elliptocytosis.