RIPK3 and colorectal carcinoma: 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.