Relationship between hemostatic gene function, physical inactivity, LPP1 and risk of deep venous thrombosis. Human skeletal muscle expresses distinct groups of genes involved in hemostasis (fibrinolysis, anti-coagulation, and coagulation factors, and enzymes involved in the synthesis of these factors). Of all these genes expressed in skeletal muscle, only LPP1 expression was affected by physical inactivity (i.e., sitting in humans). Sitting in humans and the removal of standing in rats suppressed LPP1 expression in skeletal muscle tissue. Prior studies have indicated that DVT is a complex disorder and caused by many interacting factors. We propose the novel hypothesis that the local gene expression deep in skeletal muscle could be a contributing factor. Many candidate genes known to regulate platelet aggregation and fibrin deposition are presently reported to be expressed in muscle tissues (Tables1 and2) and are presented here as four distinct groups. While some of those could be regulated post-transcriptionally, LPP1 mRNA was significantly decreased by physical inactivity. Prior published work indicates that LPP1 attenuates platelet aggregation, fibrin deposition, and inflammation. Ordinary non-exercise movements and standing, unlike the less frequent and higher intensity type of exercise more commonly associated with a boost in muscular strength or cardiovascular fitness, prevent the decrease in LPP1 expression. Items in red would favor a prothrombotic state while those in blue would be anti-thrombotic.