Gattinoni et al. (2017) already suggested this energy to be potentially harmful for the pulmonary tissue, as it is not reused for elastic recoil properties. Persistent septal micro injury may be, in turn, a relevant factor for altered AEC2 biology, aberrant wound repair, pulmonary inflammation and interstitial fibrotic remodeling. Phenomena described in a number of children suffering interstitial lung disease (chILD), who showed reduced or absent levels of mature SP-C (Cong et al., 2017), as described in the next sections. This evidence concerns the gene SFTPC and interstitial lung disease.