CNR2 and ovarian hyperstimulation syndrome: Claudio Alvarez et al in 2007 also demonstrated that the effects of Cb2 were attributable to VEGFR-2 dephosphorylation and concluded that Cb2 may provide a new, specific and non-toxic approach to the treatment of OHSS, by which the increased vascular permeability, which is mediated by the VEGF/VEGR2 pathway, is blocked without altering angiogenesis.[5]