Cancerous growth is one of the most difficult diseases to target as there is no 
one clear cause, and targeting only one pathway does not generally produce 
quantifiable improvement. For a truly effective cancer therapy, multiple 
pathways must be targeted at the same time. One way to do this is to find a gene 
that is associated with several pathways; this approach expands the 
possibilities for disease targeting and enables multiple points of attack rather 
than one fixed point, which does not allow treatment to evolve over time as 
cancer does. Inducing programmed cell death (PCD) is a promising method to 
prevent or inhibit the progression of tumor cells. Intricate cross talk among 
various programmed cell death pathways including cell death by apoptosis, 
necroptosis or autophagy plays a critical role in the regulation of PCD. In 
addition, the complex and overlapping patterns of signaling and lack of 
understanding of such networks between these pathways generate hurdles for 
developing effective therapeutic approaches. This review article focuses on 
targeting FLIP (Fas-associated death domain-like interleukin-1-converting 
enzyme-like inhibitory protein) signaling as a bridge between various PCD 
processes as an effective approach for cancer management.