NLRP3 and neoplasm: Subsequently, cellular stress and injury—such as mitochondrial dysfunction, ROS accumulation, K+ efflux, extracellular ATP release from injured cells, lysosomal rupture, and metabolic alterations (e.g., increased lactate and reduced pH)—along with DAMPs from necrotic tumor areas, promote NLRP3 oligomerization, assembly of the NLRP3–ASC–caspase-1 complex, and secretion of IL-1β and IL-18 [13,74,75].