To elucidate the mechanism by which HOXA11 modulates the malignant phenotype more intuitively, immunoblots from gastric cancer cell lysates treated with BBI608 have shown that BBI608 treatment resulted in a dose-dependent decrease in the HOXA11, phosphorylation level of Stat3, Stat3 itself and protein markers regarding cancer stemness (CD133, CD44, CD90, Bmi1, Nanog and Sox2), metastasis (N-cadherin, α-SMA and Twist1) and survival (Survivin) (Figure 6A and Figure S2A). This evidence concerns the gene ACTA1 and cancer.