Indeed, although Masters et al. (60) showed that TXNIP is not essential to NLRP3 activation in bone marrow-derived macrophages primed with LPS and then stimulated with S. aureus, silica, or ATP, in the setting of colitis, where an increase in oxidative stress and activation of different inflammatory pathways occur, the dissociation of TXNIP could represent one of the mechanisms underlying NLRP3 activation (59). Here, TXNIP is linked to colitis.