By crossing mutp53 R172 knock-in mice with ErbB2/Neu transgenic mice we discovered that the mutp53 R172H allele is a more potent activator of ErbB2 mammary tumorigenesis than simple loss of p53, reflected by more aggressive disease, earlier tumor onset, increased tumor multiplicity and shorter survival [17]. The gene discussed is ERBB2; the disease is neoplasm.