Pancreatic sPLA2 has been indicated as a main etiological agent of MAS, one of the worst form of neonatal lung injury, characterized by massive surfactant inactivation, lung tissue inflammation and airway obstruction [30] [31] [32] . Meconium carries high amounts of sPLA2 and bile acids that are likely to contribute to lung injury, increasing sPLA2 activity and causing further surfactant inactivation [33] . Moreover, not only the pancreatic sPLA2 but also the pulmonary isoforms of the enzyme may be involved in the syndrome, [34] as lung sPLA2 production may be boosted by the meconium-induced release of pro-inflammatory cytokines [35] [36] [37] and through a specific cross-talk between different enzyme isoforms [38] . Consistently, we have recently found raised levels of pulmonary sPLA2 in BALF of patients affected by MAS when compared to their own meconium and to control babies [39] . MAS still has a mortality rate of about 50% and sometimes requires invasive treatments as broncho-alveolar lavage using saline/surfactant solutions or extra-corporeal life support [40, 41] .