Zhong et al. (2017) reported that CD36 deletion inhibits nuclear HDAC2 expression in hepatocytes, changing the acetylation of histones binding to the monocyte chemoattractant protein-1 (MCP-1) promoters and increasing macrophage infiltration and hepatic inflammation. In a study investigating the efficiency of VPA treatment in patients with spinal muscular atrophy, non-responsiveness to the drug was linked to CD36 overexpression, which suppressed the inhibitory effect of VPA on HDACs (Garbes et al., 2012). The gene discussed is CCL2; the disease is spinal muscular atrophy.