NAAA-targeted pharmacological agents demonstrate significant therapeutic potential in the management of human inflammatory diseases.[40] Emerging research has revealed that N-acyl-ethanolamine amidase (NAAA) plays a crucial role in mitigating intestinal fibrosis through the modulation of macrophage activity.[41] Furthermore, empirical evidence indicates that NAAA expression is markedly elevated in rat alveolar macrophages.[42] Our investigation has identified a correlation between upregulated NAAA transcript levels and decreased susceptibility to neonatal respiratory distress. This evidence concerns the gene NAAA and Neonatal respiratory distress.