The pathophysiological mechanisms for the direct association between psoriasis and tobacco smoking include oxidative stress, free radical damage, increasing vascular endothelial dysfunction, immune cell activation, genetic mechanisms and interaction with key signaling pathways in psoriasis [nuclear factor kappa B (NF-κB), Janus kinase/signal transducers and activators of transcription (JAK-STAT)], and mitogen-activated protein kinase (MAPK) (36–38). The gene discussed is SOAT1; the disease is psoriasis.