However, similar to CRC, genetic mutations in tumour suppressor genes such as TP53 and cyclin-dependent kinase inhibitor 2a (CDKN2A), activating mutations in oncogenic drivers such as MYC, KRAS, cyclin E1 (CCNE1) and mutations in ATR and BRCA1 & 2, all make NSCLC a potentially ideal cancer for CHK1 inhibition. This evidence concerns the gene KRAS and cancer.