Hyper-phosphorylation of LASP1 and CRKL, one of the most prominent and specific BCR-ABL substrates and a biomarker in CML, by BCR-ABL results in a disrupted interaction between both proteins, while normal binding occurs between tyrosine 171 phosphorylated LASP1 and the SH2 domain of non-phosphorylated CRKL [85]. This evidence concerns the gene CRKL and chronic myelogenous leukemia, BCR-ABL1 positive.