Rather than focusing on particular potential cleavage events, we studied the development of HD symptoms in the well-validated YAC128 murine model of HD [36-38] when bred to casp2 -/- mice [39] to determine whether developmental and complete lack of casp2 may in some way modify the phenotype of HD, without relying on proxy makers for caspase activation. The gene discussed is CASP2; the disease is Huntington disease.