It has been found that NOD1 activation contributes to tumor suppression mainly through RIP2/TAK1/MAPK pathway-mediated apoptosis in oral cancer [45], thyroid cancer [23], breast cancer [26], and GC 27, whereas NOD1 overexpression is associated with tumor development with decreased chemotherapy sensitivity but enhanced immunosuppression in HNSCC 24, ESCC25, prostate cancer [33], and ovarian cancer [36]. This evidence concerns the gene RIPK2 and ovarian cancer.