This suggests that these 3 mutations, typically considered mutually exclusive [4,12,16], can coexist in some cases of NSCLC that become resistant to crizotinib in vivo, presumably because the tumor cells or heterogeneous tumor clones utilize EGFR and/or KRAS signaling to circumvent the inhibition of ALK-mediated signaling by crizotinib. This evidence concerns the gene KRAS and non-small cell lung carcinoma.