We demonstrate that the N-end rule–based PROTACs with distinct amino acids (Arg, Lys, Leu, and Phe) easily provide a range of BCR–ABL concentration under the same condition (Fig. 4), and the Arg-PEG1-Dasa can effectively suppress BCR–ABL–induced tumor growth without overt drug toxicity in vivo (Fig. 6). The gene discussed is ABL1; the disease is neoplasm.