Apoptosis is dependent upon caspase activation leading to substrate cleavage 
and, ultimately, cell death. Although required for the apoptotic phenotype, it 
has become apparent that cells frequently die even when caspase function is 
blocked. This process, termed caspase-independent cell death (CICD), occurs in 
response to most intrinsic apoptotic cues, provided that mitochondrial outer 
membrane permeabilization has occurred. Death receptor ligation can also trigger 
a form of CICD termed necroptosis. In this review, we will examine the molecular 
mechanisms governing CICD, highlight recent findings demonstrating recovery from 
conditions of CICD and discuss potential pathophysiological functions of these 
processes.