A translocation between chromosomes 5 and 14 in patients with acute B lymphocytic leukemia resulted in the juxtaposition of the IL-3 gene and the immunoglobulin heavy-chain gene, causing overproduction production of IL-3, leading to blood and tissue eosinophilia. Primary immunodeficiency diseases
Primary immunodeficiency diseases are inborn errors in the immune system due to defective genes. Certain of these disorders are sometimes or often associated with hypereosinophilia. The list of such disorders includes ZAP70 deficiency (defective  ZAP70 gene), CD3gamma chain deficiency (defective CD3G gene), MCHII deficiency (defective RFXANK gene), Wiskott–Aldrich syndrome (defective WAS gene), IPEX syndrome (defective IPEX gene), CD40 gene defect, and autoimmune lymphoproliferative syndrome (defective Fas receptor gene). More than 30 other primary immunodeficiency diseases are sometimes associated with modest increases in eosinophil counts, i.e. eosinophilia. The hyperimmunoglobulin E syndrome is associated with hypereosinophilia or eosinophilia due to mutations in any one of the following genes: STAT3, DOCK8, PGM3, SPINK5, and TYK2 (see mutations in the hymperimmoglobulin E syndrome). Omenn syndrome is a severe combined immunodeficiency disease characterized by skin rash, slenomegaly, and lymphadenopathy due to a causative mutation in RAG1, RAG2, or, more rarely, one of several other genes. Lymphocyte-variant hypereosinophilia
Lymphocyte-variant hypereosinophilia is a disorder attributed to the expansion of a cytokine-producing, aberrant population of a particular T-cell phenotype. The disorder is clonal with regard to the
production of abnormal T-cell lymphocytes not eosinophils which appear phenotypically normal.
II is the Roman numeral for 2.