Regulating the levels of antiapoptotic and preapoptotic proteins can sensitize cells to undergo apoptosis in response to chemotherapeutic agents. Using antisense oligonucleotides, Taylor et al. have altered splice-site selection in an endogenous apoptosis gene, bcl-x (see p. 1097 and p. 1065). This treatment favors the production of a longer form of the mRNA, encoding for the proapoptotic protein (Bcl-xS), whereas it disfavors production of the antiapoptotic longer form (Bcl-xL) and sensitizes the cells to apoptotic stimuli.