For instance, circ‐ITGA7 up‐regulated its linear isoform ITGA7 via the miR‐370‐3p/neurofibromin 1/Ras pathway in colorectal cancer.11 circ‐FLI1 was capable of directly interacting with TET1 and DNMT1 to coordinately increase FLI1 expression in breast cancer.12 circ‐PABPN1 was reported to inhibit the translation of PABPN1 by reducing the binding of HuR and PABPN1 mRNA.13 These studies imply that there is a crosstalk between circRNA and its host gene. The gene discussed is FLI1; the disease is colorectal cancer.