Immunohistochemistry probing for the apoptotic marker caspase-3 revealed that tumor cell survival is dependent on tenascin C. In order to specify the effect of tumor endogenous protein production, Oskarsson et al. used an inducible knockdown model narrowing down the time frame for the dependency on tumor-derived tenascin C. Interestingly, depriving the breast cancer cells of tenascin C only affected the outgrowth of metastases when they reached a certain size (23). The gene discussed is CASP3; the disease is breast cancer.