It is known that the activation of p53 upon nucleolar stress requires the interactions of RPL5/RPL11 with MDM2 and the consequent inhibition of MDM2.[29, 30, 31, 32, 42, 43] This is also evidenced by the fact that cancer cells expressing an MDM2 mutant that cannot bind to RPL5 and RPL11 display resistance to p53 activation induced by nucleolar stress.[14] We then elucidated whether knockdown of BRIX1 activated the p53 pathway through RPL5 and RPL11. The gene discussed is TP53; the disease is cancer.