This is congruent with the findings that prolonged treatment with B1R antagonists prevented the infiltration of macrophages and other immune cells in retina, pancreas, and adipose tissue, a mechanism which can contribute to the therapeutic effects of B1R antagonism in diabetic retinopathy, insulin resistance, and other diabetic complications (Dias et al., 2010; Dias and Couture, 2012b; Pouliot et al., 2012; Tidjane et al., 2015, 2016; Talbot et al., 2016). The gene discussed is BDKRB1; the disease is diabetic retinopathy.