Besides, we examined the phosphorylation of STAT3, AKT, smad2, and smad3 as well as β-catenin, which were always activated in tumorigenesis and progression.17–20 As shown in Figure 2c, after WYC-209 treatment, the expression levels of p-STAT3, p-AKT, p-smad2, p-smad3, and β-catenin were all impeded significantly (**P < .01, *P < .05), further pointed out that WYC-209 could suppress tumor progression and was potential for antitumor therapy. Here, AKT1 is linked to neoplasm.