The study showed that exposure to extracellular components promoted KrasG12D-initiated tumorigenesis, although environmental exposure did not consistently correlate with tumor formation, such as that in the small intestine, suggesting the presence of intrinsic differences in susceptibility to Kras activation and that tumor susceptibility is not limited to the epithelial cells but is different depending on the cellular context (16). This evidence concerns the gene KRAS and neoplasm.