Paclitaxel is an antimicrotubule agent that is known to target β-tubulin subunits. Ferlini and colleagues have demonstrated that paclitaxel also interacts with Bcl-2, and is able to convert its function from antiapoptotic to proapoptotic. The direct interaction was proven with surface plasmon resonance technology (biosensogram, bottom panel ). Using bioinformatics, modeling of the interaction was obtained (top panel ) and, through this approach, the authors discovered an extraordinary homology between the binding site in both paclitaxel targets (Bcl-2 and β-tubulin). This finding suggests the possibility that paclitaxel is a peptide-mimicking drug. The authors assessed this possibility and discovered that the mimicked protein is Nur77, a factor known for its ability to convert Bcl-2 from a protector to a cell killer. This discovery could lead to the development of better clinical use of paclitaxel, as well as a novel generation of anticancer agents sharing this mechanism of action. For additional information, please see the article by Ferlini and colleagues on page 6906 of this issue.