Autophagy and apoptosis are two types of programmed cell death. Although autophagy and apoptosis are significantly different in morphological characteristics, there is some correlation between them. Recent research has shown that, in some cases, these two mechanisms can antagonize or promote each other, can coexist in the same cell one after another or at the same time, and have overlapped molecules. These molecules play positive or negative roles in the mechanisms of autophagy and apoptosis [25]. For example, many proteins such as Beclin1, ATG4, and ATG5 are involved in the regulatory network of autophagy and apoptosis in mammals [26]. Lépine found that ATG5 cleaves tATG5-N (24KDa) in neutrophils. Full experimental evidence has shown that ATG5 (33KDa in full-length) not only is involved in the formation of autophagy, but also can be lysed by Calpine and generate related amino-terminal lysate targeting mitochondria, truncated ATG5 (1-193) (tATG5-N), which promotes apoptosis [27]. Lépine also studied whether tATG5-N can regulate the apoptosis and found that its enhanced expression induces apoptosis. Unlike ATG-5, which is full-length, tATG5-N can shift to the mitochondria, suggesting that lysis occurs in the activated upstream of B-cell lymphoma protein 2 (B-cell Lymphoma Protein2, Bcl-2), so it appears that truncated tATG5-N can promote the release of cytochrome C from mitochondria to the cytoplasm, thereby inducing apoptosis.