Ribosomal protein (RP) is abnormally expressed in various tumors, and affects apoptosis, senescence, growth, invasion, drug and radiation therapy resistance of tumor cells through various mechanisms. The expression level of RP in tumors is closely related to the pathological grade and clinical stage of the tumor, and it becomes a potential indicator for tumor diagnosis, treatment and prognosis. RP can be modified by phosphorylation or the like to change its activity and mode of action in tumor development. The mechanism of action of RP is different from that of chemotherapy drugs, which can regulate the sensitivity of tumor cells to drugs, so as to reverse the multi-drug resistance of tumor cells in a low-toxicity and effective way. By regulating the RP to redistribute the cell cycle, the cell cycle of the tumor is arrested in the G0-G1 phase, reducing the proportion of cells in the G2-M phase. The RNA polymerase I protease involved in RP synthesis was used as a target to indirectly regulate the treatment of RP, and showed significant antitumor activity in animal models. The drug acting on RP has no obvious cytotoxicity due to its direct effect on the genome, and has low genotoxicity to the differentiated mature normal tissue cells and has better targeting. Obviously, tumor treatment for RP is highly specific and can effectively reverse multidrug resistance and radio-sensitization, providing a potentially low-toxic treatment.