Not surprisingly, the death of a cell is a complex and well controlled process. 
For several decades, apoptosis, the first genetically programmed death process 
to be identified has taken centre stage as the principal mechanism of programmed 
cell death (type I cell death) in mammalian tissues. Apoptosis has been 
extensively studied and its contribution to the pathogenesis of disease well 
documented. However, apoptosis does not function alone in determining the fate 
of a cell. More recently, autophagy, a process in which de novo formed membrane 
enclosed vesicles engulf and consume cellular components, has been shown to 
engage in complex interplay with apoptosis. As a result, cell death has been 
subdivided into the categories apoptosis (Type I), autophagic cell death (Type 
II), and necrosis (Type III). The boundary between Type I and II cell death is 
not completely clear and as we will discuss in this review and perhaps a 
discrete difference does not exist, due to intrinsic factors among different 
cell types and crosstalk among organelles within each cell type. Apoptosis may 
begin with autophagy and autophagy can often end with apoptosis, inhibition or a 
blockade of caspase activity may lead a cell to default into Type II cell death 
from Type I.