In vitro studies exhibited that fibroblasts from systemic sclerosis patients express high levels of α-SMA and CAMs (αvβ3 and αvβ5 integrin) that leads to sustained activation of the TGF-β pathway [97], as well as proinflammatory and chemotaxis cytokines such as IL-6, TNF-α, IL-1α, IL-1β, and MCP-1 [98–100]. This evidence concerns the gene CCL2 and systemic sclerosis.