Aberrant IL-33 signaling has been implicated in various lung diseases, including chronic obstructive pulmonary disease, asthma, and allergic and airway inflammatory disorders.12 In a murine model of hypoxia-induced PH, IL-33 has been shown to exacerbate vascular remodeling under hypoxic conditions.13 In addition, IL-33 signaling stimulates the proliferation of control pulmonary arterial EC (PAEC), while blockade of the membrane-bound ST2 receptor (ST2L) reduces these effects in a Sugen/hypoxia mouse model.14 This evidence concerns the gene IL33 and asthma.