In line with the overall percentage of effectors, dexamethasone also induced stronger reversion of individual proteins, such as chemokines and chemokine receptors (CCL19, CCL3, CCR2, CXCL10, CXCL2 and CXCR4), interleukins (IFNγ, IL-17A, IL-1 β, IL-7 and IL-8), and pulmonary damage (E-selectin–SELE–and P-selectin–SELP) and fibrosis effectors (MMP3, PDGFA, TNF and DR5). The gene discussed is CXCL2; the disease is fibrosis.