We observed that LOXL3-WT, but not LOXL3-K35/K36A mutant, could rescue the lipid peroxidation level (Fig. 2h, i), cell death level, drug response status (Supplementary Fig. 2i, j) and DHODH protein level (Fig. 2j) under the treatment of Oxaliplatin, which eventually excluded the canonical function of LOXL3 in chemoresistance of liver cancer. The gene discussed is LOXL3; the disease is liver cancer.