As previous studies demonstrated host cell transcriptional upregulation of AREG in response to bacterial infections with Shigella flexneri, enterohemorrhagic Escherichia coli, and Helicobacter pylori [20–22] as well as increased proteolytic cleavage of pro-AREG upon infection with Neisseria gonorrhoeae [23], we hypothesized that AREG might contribute to the reduced PICD of neonatal monocytes by affecting extrinsic apoptosis signaling. The gene discussed is AREG; the disease is bacterial infectious disease.