In the last decade, it has been well established that programmed cell death (PCD) is not confined to apoptosis (type-I PCD) but cells may use different mechanisms of active self-destruction. One such mechanism is autophagy also called as type-II PCD, which is characterized by different morphological and biochemical features. It is not surprising that the demise of a cell either by PCD-I or by PCD-II is a well-controlled and complex process. The functional role of autophagy is not confined to the cell death through PCD-II, but interestingly it can also lead to cell death through apoptosis by enhancing the caspase activation. Autophagy may also act as a cell survival process by acting as a stress response, delaying caspase activation, and removing damaged organelles. Therefore, the crosstalk between apoptosis and autophagy is quite complex and sometimes contradictory as well, but unquestionably it is decisive to the overall fate of the cell. The molecular regulators of both pathways are inter-connected, and both share some factors that are critical for their respective execution. B-cell lymphoma-2, which was well known as an anti-apoptotic protein is now also considered as an anti-autophagic. Beyond the simplistic view of caspases in apoptosis, recent studies have uncovered unexpected functions of caspases in the regulation of autophagy, indicative of the novel frontiers lying ahead in the science of autophagy.