Although KDM3A has been shown to specifically demethylate H3K9me2 in lung cancer, seminomas, bladder cancer and prostate cancer, it appears to indirectly control H3K4me2 in gastrointestinal tumors.[10, 11, 16] Consistently, previous research reported that increased H3K4me2 levels led to dsRNA stress and the activation of tumor‐intrinsic IFN by enhancing ERVs expression.[8g] Collectively, these findings confirm the role of KDM3A as an epigenetic regulator, influencing H3K4me2 expression and thereby modulating the MAVS‐IFN signaling pathway. The gene discussed is MAVS; the disease is urinary bladder cancer.