It has been reported that the type I interferon (IFN)‐induced chemokines, CXCL9 and CXCL10, are frequently associated with recruitment of CD8+ T lymphocytes to tumor sites.[19] It has been shown that pSTAT3 interacts with STAT1 to inhibit type I IFN response.[20] To test this possibility, we examined whether the expression of CXCL9 and CXCL10 were upregulated upon circFAT1 KD. The gene discussed is STAT1; the disease is neoplasm.