KRAS and neoplasm: Interplay between RAS signalling and suppression of interferon pathways was also implicated in a mouse KRAS-mutant lung cancer model that was engineered to have increased tumour mutational burden; KRAS-G12C inhibition reprogrammed the tumour microenvironment to favour anti-tumour immune responses with increased antigen presentation, cytokine production, interferon signalling, immune cell infiltration and T-cell activation [121].