Although previous studies revealed that the effectiveness of Taxol to ovarian cancer can be regulated by multiple pathways, including cell death related pathways, such as the JNK/SAPK pathway, the p53 pathway [33] and signaling pathways like the PI3K/AKT pathway [34, 35], the FAK/Rho pathway [36] etc., pathway analysis of RIPK2 and its coexpressed genes didn’t show enrichment in these pathways, which might suggest that RIPK2 participates in Taxol-resistant ovarian cancer by activating NF-κB mediated transcription [37]. Here, NFKB1 is linked to ovarian carcinoma.