KRAS and neoplasm: Interestingly, in 2018, Ambrogio and colleagues, by using a genetically-inducible model of K-RAS loss of heterozygosity, indicated that K-RAS dimerization mediates wild-type KRAS-dependent fitness of human and murine K-RAS mutant lung adenocarcinoma tumour cells and underlies resistance to MEK inhibition [32].