Moreover, chemoresistance of CML and chronic eosinophilic leukemia (CEL) to anticancer treatment with the multi-targeted tyrosine kinase inhibitor imatinib may occur via hypermethylation of the “phosphatase and tensin homolog deleted on chromosome 10” (PTEN) gene involved in the dephosphorylation (silencing) of AKT, ERK and STAT5 signaling pathways (Nishioka et al., 2010). This evidence concerns the gene PTEN and Chronic Eosinophilic Leukemia, Not Otherwise Specified.