It was indeed reported that Beclin-1, but also ATG5 and ATG3, are caspase-8 substrates in vitro, and that after death receptor activation in several cancer cells, the subsequent downregulation of autophagic flux is partly due to caspase-8-dependent cleavage of these autophagic proteins [32–34, 44, 45]. The gene discussed is ATG5; the disease is cancer.