OA was shown to inhibit the IL-1/NF-κB/TET3 axis in cancer cells, resulting in DNA hypomethylation and the suppression of PD-L1, thereby strengthening the robust T-cell defense mechanism.123 In addition, synthetic derivatives of OA, such as CDDO-Im, have been shown to block the EGFR/signal transducer and activator of transcription 3 (STAT3)/Sox-2 signaling pathway in tumor-associated macrophages (TAMs), which have been implicated in promoting breast cancer proliferation and metastasis.124 Thus, OA may be a potential therapeutic agent for the treatment of cancer. Here, NFKB1 is linked to neoplasm.