Bim/Bod is a pro-apoptotic protein belonging to the -BH3-only+ group of Bcl-2 family members (that includes Bad, Bid, Bik, Hrk and Noxa) containing a BH3 domain but lacking other conserved domains, BH1 or BH2 (1,2). Bim induces apoptosis by binding to and antagonizing anti-apoptotic members of the Bcl-2 family. Interactions have been observed with Bcl-2, Bcl-xL, Mcl-1, Bcl-w, Bfl-1 and BHRF-1 (1,2). Particular functions for Bim have been described in the regulation of apoptosis associated with thymocyte negative selection and following growth factor withdrawal, during which Bim expression is elevated (3-6). Three major isoforms of Bim are generated by alternative splicing: BimEL, BimL and BimS (1). The shortest form, BimS, is the most cytotoxic and is generally only transiently expressed during apoptosis. The other isoforms, BimEL and BimL, may be sequestered to the dynein motor complex through an interaction with the dynein light chain and released from this complex during apoptosis (7). Apoptotic activity of these longer isoforms may be regulated by phosphorylation (8,9). Environmental stress triggers Bim phosphorylation by JNK, resulting in dissociation with the dynein complex and increased apoptotic activity.