However, given the data resulting from the specific deletion of Sema7A in peritoneal MΦs and the image stream, protein microarray, and NMR experiments, the predominant role of Sema7A in murine peritonitis appears to be mediated through the interaction with the αvß1 integrin receptor, resulting in activation of the mTOR and AKT1 phosphorylation signaling pathways within peritoneal MΦs, which are known to be critical for regulating MΦ metabolism and polarization toward the M2 phenotype (19). The gene discussed is SEMA7A; the disease is peritonitis.