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. This evidence concerns the gene IFNA1 and Familial prostate cancer.