Our previous study showed that miR-205 overexpression in EPCs targeted PTEN, downregulated PTEN mRNA and protein expression levels, and regulated the expression of matrix metalloproteinase-2 through the AKT/autophagy pathway, thus enhancing the migration, invasion, proliferation, and angiogenesis abilities of EPCs and further accelerating the resolution and recanalization of DVT [11]. The gene discussed is AKT1; the disease is deep vein thrombosis.