Given that α-hederin retarded colorectal tumorigenesis progression was associated with inhibition of STAT3 activation (Fig. 1, 4, 5), STAT3 and phosphorylated STAT3 of paired CRC tissues were tested simultaneously, and results showed that they were also higher expressed in CRC tissues than paired normal tissues (Fig. 7D), which highlighted the indispensable role of USP5 and STAT3 in CRC development and progression. The gene discussed is STAT3; the disease is colorectal carcinoma.