The KRASG12D inhibitor MRTX1133 shows model-dependent efficacy, with variable effects in 2D cell lines, enhanced efficacy in 3D cultures, tumour growth control in patient-derived xenografts (PDX), and regression in syngeneic models; mechanistically, it acts via ITGB1 and remodels the tumour microenvironment (enhancing IFN-γ signalling, recruiting effector CD8+ T cells), thus supporting KRAS G12D inhibition as a promising PDAC strategy [82]. This evidence concerns the gene ITGB1 and neoplasm.