TP53 was attested to inactivate by mutations or deletions in most human tumors and POLR2A, an important gene close to TP53, was always deleted together with TP53. Liu et al. presented that if the expression of POLR2A was inhibited by siRNA, the proliferation, survival, and tumorigenic potential of CRC cells with hemizygous TP53 loss would be selectively inhibited in a p53‐independent manner.23 The gene discussed is TP53; the disease is colorectal carcinoma.