Bi-1 is an anti-apoptotic protein that inhibits Bax activation and its translocation to the mitochondria. Functionally, BI-1 affects the leakage of Ca2+ ions from the ER. In addition to its anti-apoptotic role, BI-1 also enhances cancer/tumor progression. It belongs to the Bcl-2 family, plays an important role in the mitochondrial apoptosis pathway. Bi-1 over-expression suppresses apoptosis induced by Bax, staurosporine and growth factor deprivation. BI-1 is presumably not needed for the physiological regulation of developmental programmed cell death. The anti-apoptotic mechanism of BI-1 involves the suppression of Bax activation and translocation to mitochondria, preserving the mitochondria membrane potential and mitochondrial morphology, and preventing the activation of post-mitochondrial caspases. BI-1 function is also associated with the regulation of intracellular Ca2+ omeostasis. In several human cancers, including nasopharyngeal carcinoma, its expression was found to be increased, however, up-regulated expression of this protein has been linked to increased cell proliferations.