Moreover, by chromatin-immunoprecipitation experiments, we demonstrated that JQ1 displaces BRD4 binding to the acetylated-histone H3 in the promoter region of the proinflammatory genes IL-6, CCL-2, and CCL-5 (Suarez-Alvarez et al., 2017), showing a mechanism involved in these anti-inflammatory properties of iBETs in experimental renal diseases (Figure 3). The gene discussed is CCL2; the disease is kidney disorder.