Cellular homeostasis is quintessential of regulated protein turnover machinery within a cell. Any form of interference with this highly orchestrated phenomenon of protein production in the Endoplasmic reticulum (ER) can induce cellular stress. The continued blockade of the ER with misfolded proteins can lead to structural abnormalities of the ER and the mitochondria, following which a cascade of cellular reactions is triggered, marked by the increase in the levels of cytosolic Ca++ and dissipation of mitochondrial membrane potential. BAX promotes the loss of membrane potential of the mitochondria causing the release of Cytochrome-c and to counter it, BAX-inhibitor (BI-1) plays a crucial role in protecting the cell from undergoing programmed cell death (PCD). A homolog of BI-1 from Plasmodium Spp. has been identified in the Toxoplasma genome (TgBI-1), which we intend to characterize by inducing stress on the parasite cell and then by reversibly modulating the levels of the concerned protein (putative BI-1) by using a tunable system like transactivator (Tet-off) to observe the repercussions in the cellular behaviour.