To better assess the role of mitochondria in inflammasome activation, we measured the level of CASP-1, IL-1β and IL-18 in PBMC from CKD-HD stimulated with LPS/ATP, Pathogen-associated molecular pattern (PAMP) and danger-associated molecular pattern (DAMP) signals able to activate NLRP3 inflammasome, in absence or presence of mitoTEMPO, an inhibitor of mitochondrial ROS production. This evidence concerns the gene CASP1 and Huntington disease.