While there is some evidence showing that p73 haploinsufficiency may cause neurodegeneration in mouse models by modulation of tau kinases, we found no evidence for robust tau pathologies in tissue sections and in biochemical fractionations of cell lysates from Trp73 haploinsufficient mice that deposit human Aβ peptide, nor in aged deltaNp73 homozygous null mice, nor any evidence that variants in the human TP73 gene influence AD susceptibility. The gene discussed is TP73; the disease is Alzheimer disease.