We have complemented ‘inhibitor time courses’ with ‘inhibitor wash-out’ experiments as an experimental paradigm to study ERK reactivation and show that the type of response in both assays correlate well with sensitization to inhibitors in viability assays: In the absence of SHOC2, feedback relief mediated ERK-activation is selectively impaired in KRAS- and EGFR-mutant NSCLC cell lines treated with MEK, but not RAF or ERK inhibitors (Fig. 4). Here, RAF1 is linked to non-small cell lung carcinoma.