A study in human aortic endothelial cells demonstrated that the mir-1908 was repressed at 4 Gy-72h with multiple target mRNAs (e.g., VPS37D, GBP5) induced, identifying it as a mechanistic biomarker of radiation response [Chopra et al. DOI:10.1038/s41598-022-24051-6]. A study in rats demonstrated that the mir-1908 is upregulated in hypertrophic scars and targets Ski, suppressing its expression to enhance growth, collagen synthesis via increased TGF-β1, and pro-inflammatory markers (IL-1α, TNF-α), contributing to scar formation in burn models [Wang et al. DOI:10.1007/s00438-024-02183-w].