Interestingly, according to Savale et al. [34], in PAH patients treated with sotatercept the LDL receptor is upregulated compared to the placebo, indicating a compensatory mechanism due to lack of activin A. Furthermore, sotatercept, preventing activation of the Smad2/3 pathway by trapping activins or GDF11, reverses the process that leads to hematological disorders related to abnormal activin signaling. The gene discussed is INHBE; the disease is pulmonary arterial hypertension.