By controlling HIF-1α activation in PASMCs under hypoxia or possibly during chronic lung diseases, which may lower local O2 tension, CD146-mediated NF-kB expands its well-established proinflammatory function, because HIF-1α-dependent hypoxic response is critical for providing PASMCs and maybe other types of pulmonary cells undergoing hypoxia with sufficient energy supplies and allows them to resist cell death and apoptosis. This evidence concerns the gene HIF1A and chronic lung disease.