Many cancer therapies function by activating proteins like Caspase-3 (CASP3) that promote cell death. Several forms of cancer develop resistance to these drugs by down regulating CASP3 through an unknown mechanism.
In the absence of CASP3, tumor cells produce another cell death promoting protein CASP7, but it is rendered inactive by the X-linked inhibitor of apoptosis protein (XIAP). In the Journal of Clinical Investigation, Po-Huang Liang and colleagues at Academia Sinica identify a compound (I-Lys) that disrupts the interaction between CASP7 and XIAP.