Paclitaxel is a widely used naturally occurring antineoplastic drug which has shown great promise in the treatment of breast, ovarian, lung and esophageal cancers. Paclitaxel exerts its cytotoxic effect by binding and stabilizing microtubules and induces apoptosis in a variety of tumor cells.  The mechanisms underlying paclitaxel-induced apoptosis are not entirely clear.  Morphologically, a sustained block of mitosis seems to be required for paclitaxel-induced apoptosis because most apoptotic events are observed to occur in cells showing a prior mitotic arrest.  However, this morphological correlation alone does not prove that paclitaxel-induced apoptosis is indeed a secondary event resulting from mitotic arrest.  Instead, several lines of evidence obtained from recent studies indicate that apoptotic cell death induced by paclitaxel may occur via signaling pathways independent of microtubules and G2/M arrest.  A number of apoptosis-associated genes and regulatory proteins have been identified to be activated or regulated by paclitaxel.  Morevoer, recent studies have suggested that the NF-κB/IκBα signaling pathway might play an active role in the mediation of paclitaxel-induced apoptosis in solid tumor cells.