NLRP3 and neoplasm: High glucose increases NLRP3 activation, probably involved in ICIs-induced resistance and cardiotoxicity; in fact, recently, a mechanism was identified whereby CD8+ T cell activation in response to PD-1 blockade induced a NLRP3 inflammasome signaling cascade that ultimately led to the recruitment of granulocytic myeloid-derived suppressor cells (MDSCs) into tumor tissues, thereby dampening the resulting antitumor immune response [75].