Using a genetically engineered mouse model heterozygous for p53 (p53+/-) crossed with JNK knockout (JNK1-/- or JNK2-/-) animals, Cellurale et al demonstrated that the resulting p53+/;JNK1-/- and p53+/-;JNK2-/- mice had reduced tumor-free survival compared to p53+/- mice that express wildtype JNK [26]. The gene discussed is MAPK9; the disease is neoplasm.