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We explored the effects of imatinib mesylate, an inhibitor of Bcr\u2013Abl protein used in front\u2010line CML therapy, on the adhesivity of JURL\u2010MK1 cells to fibronectin and searched for underlying changes in the cell proteome. As imatinib induces apoptosis of JURL\u2010MK1 cells, we used three different caspase inhibitors to discriminate between direct consequences of Bcr\u2013Abl inhibition and secondary changes related to the apoptosis. Imatinib treatment caused a transient increase in JURL\u2010MK1 cell adhesivity to fibronectin, possibly due to the switch off of Bcr\u2013Abl activity. Subsequently, we observed a number of changes including a decrease in cell adhesivity, F\u2010actin decomposition, reduction of integrin \u03b21, CD44, and paxillin expression levels and a marked increase in cofilin phophorylation at Ser3. These events were generally related to the proceeding apoptosis but they differed in their sensitivity to the individual caspase inhibitors. J. Cell. 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