Earlier studies have reported that KLF2 can modulate proinflammatory gene expression in monocytes and endothelial cells (89–91), and our findings suggest a role for KLF2 in driving tumor epithelial cell programs possibly involving paracrine cell signaling pathways (e.g., exosome-derived miRNAs; refs. 92–95). Here, KLF2 is linked to neoplasm.