At relatively high concentrations (> 4 μM), Chal-24 activates autophagy through JNK-mediated phosphorylation of Bcl-2 and Bcl-xL, leading to disruption of the Beclin1/Bcl-2 and Beclin1/Bcl-xL complexes, with subsequent degradation of the c-IAP proteins and formation of the Ripoptosome complex, resulting in necroptosis in cancer cells [17]. Here, BCL2L1 is linked to cancer.