To gain insight into the molecular mechanism of TCRζ deficiency in CML, we analyzed the distribution of the TCRζ 3'-UTR isoforms, which contribute to the regulation of TCRζ expression[19], and the ASF/SF-2 gene expression level, which regulates the alternative splicing of eukaryotic genes. This evidence concerns the gene SRSF1 and chronic myelogenous leukemia, BCR-ABL1 positive.