Background & Objective: A fundamental characteristic of cancer cells is to survive induction of apoptosis, which is a major killing mechanism of cancer cells by therapeutic agents. Gastric adenocarcinoma, like many other malignancies, is usually unresponsive to available chemotherapeutic agents. This is believed to be primarily due to resistance of gastric adenocarcinoma cells to apoptosis. The BH3-only proteins of the Bcl-2 family play a critical role in regulating the mitochondria-mediated "intrinsic apoptotic pathway" by acting as "sensor" proteins. Among them, the microtuble-associated protein Bim has been demonstrated to be critical in induction of apoptosis by microtubule-targeting agents in some types of cancers such as breast and non-small-cell-lung cancers. To better understand the biological basis for resistance of gastric adenocarcinoma to microtubule-targeting agents and explore the effective approaches for overcoming resistance of cancer cells to apoptosis, the current study examined the mechanism(s) by which paclitaxel induces apoptosis of cultured gastric adenocarcinoma cells, and in particular, the potential role of Bim in determining sensitivity of gastric adenocarcinoma cells to paclitaxel-induced apoptosis.Method: SGC-7901 and BGC-823 gastric adenocarcinoma cells were treated with paclitaxel at varying doses for different time periods. The levels of apoptosis were quantitated using Annexin V  staing in flowcytometry.  The role of caspases in