KRAS and neoplasm: These efforts include; (i) approaches that are based on inhibiting signal transduction pathways that act downstream of KRAS, such as the use of MEK inhibitors [13], (ii) the identification of synthetic lethal (SL) interactions with mutant KRAS [14–21] and, (iii) direct small molecule inhibition of KRAS, an approach that exploits the presence of a mutant cysteine residue in KRAS mutant tumour cells with p.G12C mutations [22].