In cell studies, MRTX-1133 exhibited a concentration-dependent inhibition of key KRAS pathway signaling molecules in KRASG12D mutated HPAC (pancreatic cancer) and GP2D (colorectal cancer) cell lines, including the phosphorylation of extracellular signal-regulated kinase 1/2 (pERK), the phosphorylation of S6 (pS6), the phosphorylation of 4EBP1 (p4EBP1), and the expression of dual specificity phosphatase 4 or 6 (DUSP4/6). This evidence concerns the gene KRAS and pancreatic neoplasm.