In our study, the role of ER stress in the NEC brain seems to be non-protective due to the increased levels of BiP and CHOP proteins that mediate ER stress-associated apoptosis [25, 38, 39], the increase in CC3 protein that mediates programmed cell death, and the presence of pro-inflammatory amoeboid microglia. This evidence concerns the gene HSPA5 and necrotizing enterocolitis.