Considering the integral role of the inflammatory milieu in ICC pathogenesis,[36] with NF‐κB acting at the core of inflammation‐mediated cellular functions and chemoresistance, this finding is particularly compelling.[38] Typically, the NF‐κB complex is held in check by IκBα,[39] which obscures the complex's nuclear entry signal, thus inhibiting its nuclear transcriptional activities.[40] This body of work not only highlights the potential of circPCSK6 as a critical element in the molecular landscape of ICC but also opens the door for novel therapeutic strategies targeting this pathway. This evidence concerns the gene NFKB1 and intrahepatic cholangiocarcinoma.