SCRN2 and cancer: DNA methylation is a general epigenetic mechanism involved in gene silencing in human cancer.[29] To examine whether abnormal epigenetic methylation contributes to SCRN2 downregulation in TNBC, we first analyzed the CpG islands of SCRN2 promoter (from ‐1000 bp to +100 bp relative to transcription start site) using the MethPrimer program (http://www.urogene.org/index.html).[32] Following the established criteria of CpG island size > 100 bp, GC percentage > 50%, and observed/expected CpG ratio > 0.6,[33] we detected a CpG island in SCRN2 promoter (Figure S4A, Supporting Information).