The proapoptotic protein Bim is expressed de novo following withdrawal of serum survival factors. Here, we show that Bim−/− fibroblasts and epithelial cells exhibit reduced cell death following serum withdrawal in comparison with their wild‐type counterparts. In viable cells, Bax associates with Bcl‐2, Bcl‐x_L and Mcl‐1. Upon serum withdrawal, newly expressed Bim_EL associates with Bcl‐x_L and Mcl‐1, coinciding with the dissociation of Bax from these proteins. Survival factors can prevent association of Bim with pro‐survival proteins by preventing Bim expression. However, we now show that even preformed Bim_EL/Mcl‐1 and Bim_EL/Bcl‐x_L complexes can be rapidly dissociated following activation of ERK1/2 by survival factors. The dissociation of Bim from Mcl‐1 is specific for Bim_EL and requires ERK1/2‐dependent phosphorylation of Bim_EL at Ser⁶⁵. Finally, ERK1/2‐dependent dissociation of Bim_EL from Mcl‐1 and Bcl‐x_L may play a role in regulating Bim_EL degradation, since mutations in the Bim_EL BH3 domain that disrupt binding to Mcl‐1 cause increased turnover of Bim_EL. These results provide new insights into the role of Bim in cell death and its regulation by the ERK1/2 survival pathway.