Then, the R‐Smads and Co‐Smads, SMAD4, formed a heterodimeric complex that is transferred into the nucleus and, together with other transcription factors, regulated the expression of the target gene.28 Qiao et al29 informed that miR‐34a repressed EMT in human cholangiocarcinoma by directing SMAD4 through the TGF‐β/Smad signaling pathway. This evidence concerns the gene TGFB1 and cholangiocarcinoma.