Mechanistic studies have showed that circACTN4 can disrupt the interaction between far upstream element binding protein 1 (FUBP1) and poly (U) binding splicing factor 60 (FIR) by competitively binding to FUBP1 and subsequently enhancing the MYC transcription level, which contributes to breast cancer progression [64]. This evidence concerns the gene FUBP1 and breast cancer.