Consistent with this, genetically engineered mouse models show that ALK4 deletion in combination with oncogenic KRAS drives pancreatic tumorigenesis25,26, and CRISPR-Cas9-mediated ALK4 depletion enhances colon cancer tumorigenicity in the presence of APC and KRAS mutations27. This evidence concerns the gene ACVR1B and malignant colon neoplasm.