Clinical trials evaluating MEK inhibition alongside PD-1/L1 therapy (Fig. 1) in KRAS-mutant tumours had limited success, ostensibly due to tumour heterogenicity and MEK inhibition of CD8 + T cell IL-2 production, which is crucial for clonal expansion and leads to an exhausted phenotype, inhibiting the adaptive immune response [14, 32]. This evidence concerns the gene KRAS and neoplasm.