Moreover, C. acnes can induce inflammatory response by activating the innate immune system via the Toll-like receptors TLR2 and TLR4, and by activating the NF-κB, MAPK and NLRP3 inflammasome signaling pathways, leading to production of the proinflammatory molecules IL-1α/β, IL-6, CXCL8/IL-8, IL-12, granulocyte-macrophage colony-stimulating factor (GM-CSF), TNF-α, β-defensin-2 (hBD-2), and matrix metalloproteases (MMPs) by keratinocytes, sebocytes and monocytes in vitro and ex vivo, in acne lesions [17,18,19,20,21,22,23]. The gene discussed is CSF2; the disease is acne.