Indeed SP-B and SP-C protein levels are crucial in the adaptation of the newborn at extrauterine conditions (55) as illustrated by SP-B deficiency causing severe neonatal respiratory distress and death within the first few months of life (56) whereas chILD is mainly triggered by surfactant metabolism disruption due to abnormal proSP-C protein together with decrease ABCA3, SP-C and SP-B levels (57). The gene discussed is SFTPC; the disease is interstitial lung disease specific to childhood.