Because expression of the BH3-only protein NOXA as well as the pro-apoptotic effector BOK22 is enhanced by proteasome inhibition, we hypothesized that reducing the anti-apoptotic capacity by ABT-199 and simultaneously enhancing the pro-apoptotic activity of NOXA and BOK by the proteasome inhibitor BZB might be a rational strategy in STS. The gene discussed is PMAIP1; the disease is telomere syndrome.