A previous study showed that the small molecule cytosporone B (Csn‐B) could indirectly impede the Nur77‐PPARγ interaction by promoting Nur77 homodimer formation, which in turn led to steric hindrance to prevent PPARγ binding.[6] Given the pivotal role of mono Nur77 in breast cancer, directly inhibiting the Nur77‐PPARγ interaction would be extremely valuable for promoting mono Nur77 accumulation and binding to transcriptional corepressors to downregulate CD36 and FABP4 expression. The gene discussed is NR4A1; the disease is breast carcinoma.