In this study, we found that in addition to the change in IMPA2/AIFM2 expression in paclitaxel-treated cells, the expression of p53 also increased with increasing drug concentration, suggesting that p53 is also involved in regulating paclitaxel-induced apoptosis in cervical cancer cells, i.e., IMPA2/AIFM2/p53 may be a new molecular mechanism for the development of paclitaxel resistance and a potential new target for paclitaxel sensitization therapy. Here, TP53 is linked to cervical carcinoma.