In order to examine the CRC-specific function of PrxII in vivo, we generated double-mutant mice by mating PrxI+/− and PrxII+/− mice with APCMin/+ mice, which develop multiple intestinal neoplasia (Min) by APC truncation mutation (Supplementary Fig. 1a–c). This evidence concerns the gene PRDX1 and colorectal carcinoma.