In addition, Simpson et al. (35) used RSV to inoculate primary human AECs and found that HMGB1 levels were increased in nasopharyngeal specimens from children with RVS infection and that RSV induced epithelial cell death and increased phosphorylated RIPK1 and MLKL levels, whereas RIPK1 or MLKL inhibition attenuated the RSV-induced translocation and release of HMGB1 and reduced the viral load, further indicating that RSV is involved in the pathogenesis of bronchiolitis through NEC. This evidence concerns the gene RIPK1 and bronchiolitis.