FOXP3 and neoplasm: While Wang and colleagues abolished RUNX1 expression in an immortalized cell line (MCF10-A-5E) [12], we reduced RUNX1 transcriptional activity in tumor cell lines (LM3 and MDA-DB-231) and upregulated its endogenous functional availability in normal epithelial cell line (SCp2) by RUNX1 overexpression or Foxp3 knockdown.