The opening of MLKL pore contributed to potassium efflux, activating NLRP3 inflammasomes.[202] Furthermore, the ZBP1 protein functioned as an endogenous/viral nucleic acid ligand sensor, which modulated innate immune responses.[203] Upon its activation, RIPK3 and caspase‐8 were recruited to stimulate NLRP3 inflammasomes, resulting in necrosis and pyroptosis.[204] Another study highlighted the impact of elesclomol treatment on CRC cells, which caused an elevation in mitochondrial Cu(II) levels and reduced the expression of Cu(II) transporter ATP7A, promoting ROS buildup. This evidence concerns the gene MLKL and colorectal carcinoma.