In this regard, it can be speculated that pneumocyte hypertrophy caused by HDM-allergy might alter the expression of cell surface receptors mediating pneumocyte-AMØ interactions, such as CD200 and CD47, and compromise Gap junction-mediated bi-directional metabolic communication between pneumocytes and AMØs (42), that could ultimately lead to AMØ detachment from alveolar epithelial cells and AMØ death. The gene discussed is CD177; the disease is allergic disease.