The genomic landscape of lung cancers is markedly different between never smokers and smokers, with: the non-smokers showing a lower tumor mutational burden, a predominant transition of cytosine to thymine (C > T) and a higher frequency of actionable driving gene alterations, such as EGFR mutations and ALK and ROS1 fusions; the smokers exhibiting a clearly higher mutation burden, predominantly cytosine to adenine (C > A) nucleotide transversions and non-actionable mutations, such as KRAS and TP53 mutations. The gene discussed is KRAS; the disease is neoplasm.