34 demonstrated the involvement of autophagic cell death in lung adenocarcinoma cells induced by sulindac sulfide amide treatment. Intriguingly, cell death occurred in this system was independent of caspase activation 34. Meanwhile, Lamy et al. 35 proved that autophagic activity in myeloma cells was restricted to the cleavage of an autophagic inducer, BCL2 interacting protein BCLAF1 and then cell death could be avoided. Furthermore, SI113, worked as an SGK1 inhibitor, could also induce cytotoxic autophagy in human glioblastoma multiforme cells 36. This evidence concerns the gene BCLAF1 and lung adenocarcinoma.