We genetically confirmed that the effect of systemic BBI608 administration could, at least in part, be due to tumor-cell-intrinsic STAT3 signaling because CRISPR-Cas9-mediated STAT3 deletion in KPT organoids (Figure 3D) reduced their growth when established as allografts in Stat3WT hosts (Figure 3E). Here, STAT3 is linked to neoplasm.