Mechanistically, the BM-MSC-mediated paracrine effects on relieving NEC are contributed by nuclear factor-κB (NF-κB) signaling, and the silencing of PHD2 in BM-MSCs enhances NF-κB activation, which further increases the paracrine release of insulin-like growth factor (IGF)-1 and transforming growth factor-beta 2 (TGF-β2) to reduce intestinal injury [25]. Here, TGFB2 is linked to necrotizing enterocolitis.