In vivo studies supporting a role of paraptosis or ACD in disease are rare, but in a mouse model investigating Alzheimer disease phenotypes, mice expressing a transgene of the p53 isoform p44 and the amyloid precursor protein were found to suffer from neurodegeneration that was caspase- and apoptosis-independent and shared morphological features assigned to paraptosis and ACD [171]. The gene discussed is APP; the disease is granular corneal dystrophy type II.