Considering that the SH3 domain of Abl is the one involved in the regulation of the leukemic cells adhesive and invasive properties, one of the hallmarks of the pathogenesis of CML[13], and knowing the role of C3G in cellular adhesion, we hypothesize that C3G could modulate CML cells adhesiveness through its interaction with Bcr-Abl at the FAs. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.