Herein we show that both PM2.5 exposure and asthma exhibited overexpression of proinflammatory cytokines such as IL-1β, TNFAIP3, G-CSF, and M-CSF (encoded by CSF3 and CSF1 genes), and several members of the CXCL family of chemokines (as CXCL2, CXCL3, CXCL8), while showing low expression of TRAF5, a gene whose deficiency enhances Th17 cells development [46]. The gene discussed is CXCL3; the disease is asthma.