Programmed cell death plays an important role in animal development, tissue 
homeostasis and eliminating harmful or virally infected cells. Necroptosis, a 
novel form of programmed cell death, is caspase independent but RIPK and RIPK3 
dependent. Moreover, it is suggested that necroptosis can be specifically 
inhibited by small molecular inhibitors such as necrostatin-1. Its signaling 
pathways have something in common with apoptosis, although the molecular 
mechanisms of necroptosis need to be further elucidated. Previous evidences 
suggest that necroptosis has significant effects in regulating various 
physiological processes and disease, such as ischemic brain injury, immune 
system disorders and cancer. In this review, the molecular mechanism of 
necroptosis is described and how it could be manipulated in the treatment of 
cancer is summarized.