While we did not monitor for these ‘cofilin rods’ in the brains of the TG2 KO crosses, the lack of amelioration of any disease phenotype in these animals suggests that TG2 activity is either not required for the formation of these rods in a physiological context, or that these rods are not relevant to disease progression in the R6/2 and zQ175 HD models. This evidence concerns the gene TGM2 and Huntington disease.