Our study provides biological basis and preclinical relevance that likely support a novel mechanism underpinning the paclitaxel resistance in ovarian cancer in vitro, in which CEPB4 is connected to the enhancement of paclitaxel resistance by its translational control of inducing CSAG2 expression, and thereby, uncovering the promotive function of CEPB4/CSAG2 axis in paclitaxel resistance in ovarian cancer. The gene discussed is CSAG2; the disease is ovarian cancer.