HDAC5 was shown to be involved in macrophage differentiation in lymphoma U937 cells (85), and HDAC5 depletion in U937 cells reduced the levels of tumor necrosis factor α (TNF-α) and monocyte chemoattractant protein 1 (MCP-1) via stimulation of NF-κB activity, suggesting a regulatory function for HDAC5 in the proinflammatory response of macrophages (62). Here, CCL2 is linked to lymphoma.