Similarly, in pancreatic organoids, dual mutations in Kras and Cdkn2a led to non-tumorigenic clones, dual mutations in Kras and Tp53 only produced tumorigenesis in the presence of cancer-associated fibroblasts and quadruple mutations in Kras, Cdkn2a, Tp53 and Smad4 led to rapid tumorigenesis [25]. The gene discussed is KRAS; the disease is cancer.