In addition, some studies have concluded that the ablative expression and/or function of MCL1 is sufficient to promote apoptosis among neutrophils and thus reduce the inflammatory response.[33,34] Within the context of IPAH pathophysiology, the divergence between these reports and our findings could be reconciled by 2 factors: the overlooked MCL1L/S isoform ratio,[35] and inherent inter-individual variability among study subjects. The gene discussed is MCL1; the disease is idiopathic pulmonary arterial hypertension.