In agreement with previous results[4,54], our data suggest that C3G plays a key role in the regulation of CML cell adhesion as (i) C3G silencing decreases adhesion to fibronectin, (ii) changes in C3G expression alters the levels of expression and activation of FA proteins, such as FAK, paxillin, CrkL, Cbl and integrin α5, and (iii) C3G silencing increases the interaction between CrkL and paxillin (difficult to observe in control cells) and decreases CrkL interaction with Bcr-Abl. The gene discussed is RAPGEF1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.