The molecular controls of autophagy appear common in eukaryotic cells from yeast to human, and autophagy may have evolved before apoptosis [35]. However, most of the work has been done on yeast, but detailed work on autophagy in mammalian cells emerging [115]. Double-membrane autophagosomes for sequestration of cytoplasmic components are derived from the ER or the plasma membrane. Tor kinase, phosphatidylinositol 3 (PI3)-kinase, a family of cysteine proteases called autophagins, and death-associated proteins function in autophagy [116,117]. Autophagic and apoptotic cell death pathways crosstalk. The product of the tumor suppressor gene Beclin1 (the human homolog of the yeast autophagy gene APG6) interacts with the anti-apoptosis regulator Bcl-2 [118]. Autophagy can block apoptosis by sequestration of mitochondria. If the capacity for autophagy is reduced, stressed cells die by apoptosis, whereas inhibition or blockade of molecules that function in apoptosis can convert the cell death process into autophagy [119]. Thus, a continuum between autophagy and apoptosis could exist.