Finally, the mechanism by which the elevated ERK activity engendered by TKI treatment of NSCLC cells enhances survival was identified as the increased ERK-dependent phosphorylation of the extra long isoform of the pro-apoptotic BH3 only Bcl-2 family member Bim (Bim EL) (Fig. 3). Here, BCL2L11 is linked to non-small cell lung carcinoma.