In contrast, PAH was diagnosed after DAA therapy initiation in 3 patients who were asymptomatic before exposure. PoH was definitively ruled out in the first patient, who had a liver fibrosis stage F3, after performing a liver ultrasound, a gastroscopy, and a measurement of transhepatic pressure gradient. However, the 2 other patients had cirrhosis with evident PoH. The clinical, functional, and hemodynamic evolution of these 3 patients after cessation of DAA therapy and specific management of PAH is reported in Table 1. Interestingly, PAH was reversible in the patient without PoH with persistent normalization of pulmonary pressure 9 months after DAA withdrawal and without PAH-targeted therapies. In addition, PAH was dramatically improved with PAH-targeted therapy but not totally reversible in the other 2 patients. Indeed, we observed a dramatic and unusual reduction of PVR by 75% in the second patient and a near-normalization of PVR (<3 WU) in the third patient.