Because intratumoral STAT3 contributed to the resistance of FAK inhibitor in tumor treatment.28 We evaluated whether defactinib stimulated the activation of intratumoral STAT3 in ESCC cells/CAFs coculture system, and found that defactinib (10 μM) upregulated the phosphorylation of STAT3 Tyr705 in KYSE410 and KYSE510 cells in the presence of CAFs #1, compared with defactinib in KYSE410 or KYSE510 cells cultured alone (Fig. 6a). This evidence concerns the gene PTK2 and neoplasm.