Notably, 17% of KRAS mutant lung adenocarcinomas harbour the G12D substitution (glycine to aspartic acid at position 12) which confers a more invasive tumour phenotype and a reduced response to anti-EGFR targeted therapies (Gallegos Ruiz et al. 2007; DuPage et al. 2009). Here, EGFR is linked to neoplasm.