Actually, there may be alternative mechanisms underlying UTP11 depletion-mediated inhibition of p53-null tumors, as nucleolar stress also elicits several RPs, such as RPL3, RPL11, and RPS14, to enhance oxidative stress and suppress cancer progression by repressing SLC7A11 expression or c-MYC activity [[60], [61], [62]]. Here, RPL11 is linked to cancer.