The contact pathway of coagulation has been implicated in the pathogenesis of venous thrombosis. Relatively little, however, is known about the the role of C1 inhibitor, the major negative regulator of this pathway, in venous thrombosis. Work led by Steven Grover and Nigel Mackman revealed that C1 inhibitor deficiency, resulting in the genetic disorder Hereditary Angioedema, causes increased contact pathway-mediated coagulation in humans and increased venous thrombosis in mice. This work was supported by critical contributions from fellow BRC lab members Tomohiro Kawano, Jun Wan, Sophia Dhrolia, Rohan Kasthuri and Alisa Wolberg. The findings, presented in the Plenary Scientific session of ASH and now published in the Journal Blood, demonstrate an important role for endogenous C1 inhibitor in limiting pathological activation of coagulation.