A study in human peripheral blood mononuclear cells demonstrated that hsa-miR-17-5p was upregulated at 1 Gy of fractionated radiation exposure [Lee et al. DOI:10.1155/2014/456323]. In human skin, the mir-17 was downregulated four days post-burn in deep partial thickness burn skin versus normal skin and was also downregulated in burn hypertrophic scar and its derived fibroblasts compared to normal fibroblasts [Siu et al. DOI:10.1111/wrr.13100]. A study in humans demonstrated that the mir-17 is down-regulated in all seven investigated aging models, including replicative senescence of endothelial, renal, and skin cells as well as organismal aging in mesenchymal stem cells, foreskin, and T-cell populations [Hackl et al. DOI:10.1111/j.1474-9726.2010.00549.x]. This down-regulation was validated by qPCR, showing up to 6-fold decreases, and correlated with increased mRNA levels of the target gene p21/CDKN1A, establishing it as a novel marker of cell aging.