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). Here, CCL2 is linked to proximal spinal muscular atrophy.