The study revealed that upon LPS priming, ABRO1 binds to NLRP3 and recruits BRISC to promote K63-dependent deubiquitination of NLRP3 [106] and that a deficiency of BRCC3/ABRO1 attenuates NLRP3-associated inflammatory diseases such as peritonitis or sepsis [107]. This evidence concerns the gene NLRP3 and Sepsis.