Recent advances in the development of covalent inhibitors of G12C, which take advantage of the cysteine 12 residue to lock the protein in its inactive GDP bound conformation, have demonstrated promising signals of activity in clinical trials and are poised to dramatically change the treatment landscape for patients with KRAS G12C mutations owing to the relative high frequency of this alteration (approximately 13% of lung cancer) [6,7,8]. This evidence concerns the gene KRAS and lung cancer.