In addition, well‐described changes in NFκB signaling [73], downregulation of anti‐apoptotic proteins such as XIAP or BCL2 [74, 75] associated sensitivity to proteasome inhibitors, an inhibition of the NFκB signaling pathway [73], the associated downregulation of anti‐apoptotic proteins such as XIAP or BCL2 [74], the mutational status of the tumor suppressor p53 [76], and aneuploidy of the cancer cells [77] indicate increased responsivity toward proteasome inhibition. The gene discussed is TP53; the disease is cancer.