In this sense, CPEB silencing ameliorates major hallmarks of PHT, such as portosystemic collateral vessel formation, mesenteric arterial hyperdynamic circulation, and several surrogate markers of disease severity, such as increased von Willebrand factor plasma levels and splenic enlargement and hyperactivation, according to animal models (Calderone et al., 2016; Figure 3). The gene discussed is CPEB1; the disease is pulmonary hypertension, primary, 1.