This leads to increased levels of phosphorylated RIPK1, RIPK3, and MLKL while targeting endoplasmic reticulum-induced autophagy limits the synthesis of CASP-8 and the degradation of phosphorylated proteins, ultimately inducing necroptotic cell death rather than apoptosis.88 Chen et al. designed a novel copper-based chalcogenide compound (CuS-NiS2) that, upon PTT activation by light irradiation, can also mediate necroptotic cell death in tumor cells through the MLKL/CAPG pathway. This evidence concerns the gene MLKL and neoplasm.