The exact pathways involved in stimulating eosinophils downstream from the fusion protein are not fully understood but may involve signaling pathways such as phosphoinositol 3-kinase, ERK 1/2, and STAT. A study in mice using only the FIP1L1-PDGFRα mutation did not result in high levels of eosinophilia, suggesting that overexpression of IL-5 may contribute to the disease seen in CEL [7]. This evidence concerns the gene IL5 and Chronic Eosinophilic Leukemia, Not Otherwise Specified.