The negative findings, different from other reports in EGFR‐mutated lung cancer with EGFR tyrosine kinase inhibitors (Ono et al., 2014; Zhou et al., 2011), may be explained by the limited benefit with the targeted therapies explored in our cohort of chemotherapy‐refractory CRC, particularly with MEK and PI3K inhibitors in the KRAS‐ and PIK3CA‐mutant populations, respectively – the latter harboring coexisting KRAS mutations known to confer primary resistance to PI3K inhibitors as single agents (Dienstmann et al., 2012). This evidence concerns the gene EGFR and lung cancer.