A recent report shows that IgA-PIGR colonization is associated with improved survival of patients with HGSC [17], and IgA transcytosis through malignant epithelial cells via the IgA-PIGR interaction elicits transcriptional changes that sensitize tumor cells to cytolytic killing by T cells; therefore, PIGR might antagonize the growth of HGSC cells by regulating coordinated tumor cell, T cell, and B cell responses. The gene discussed is CD79A; the disease is neoplasm.