Though our current data does not formally demonstrate a causal relationship between cathepsin L deletion and alteration of autophagy in Myc-driven lesions, or that the increase in tumor cell death detected in late stages of tumor progression in the MycERTAM;Bcl-xL;CTSL-deficient neoplasias is a direct consequence of altered autophagic flux in vivo, it is reasonable to suggest that these events are intertwined [54]. The gene discussed is MYC; the disease is neoplasm.