The study of the underlying biology of KRAS in patients with NSCLC could help to determine potential candidates to evaluate novel targeted agents and combinations that may allow a tailored treatment for these patients.5 In addition, the P53 tumour suppressor gene is mutated or deleted in ∼50% human cancers.6 Wild‐type (WT) P53 helps maintain genome integrity and cellular homeostasis by regulating the expression of a plethora of genes involved in the regulation of cell cycle, apoptosis, stem cell differentiation, senescence, DNA repair and metabolism.7 The gene discussed is TP53; the disease is neoplasm.