1. Identify the exact subtype(s) of sPLA2 produced and secreted into the alveoli during post-neonatal ARDS-ALI, MAS, iRDS and IRRF. This is important to know because sPLA2 inhibitors may have a different specificity for the various enzyme subtypes. In animal models, distinct sPLA2 subtypes have been associated to lung dysfunction [1, [48] [49] [50] . 2. Study the main modulators of sPLA2 expression and activity (TNFα, CCSP, SP-A and IL1). This will allow identification of possible pathway imbalances and eventually new therapeutic targets. 3 . Clarify what happen to sPLA2 and its pathway when exogenous surfactant is administered, as it usually occurs to preterm neonates. This will allow to understand if there is a link between sPLA2 activity/overexpression, the repeated need for surfactant and BPD occurrence. 4. Clarify if there is a genetic predisposition due to different sPLA2 genes polymorphisms which could lead to more severe clinical pictures in iRDS, ARDS, MAS or IRRF or to a long term negative outcome.