Both actin- and MKP-1-S-glutathionylation enhance the responsiveness of THP-1 cells to chemoattractants, and accelerate monocyte migration and adhesion, characteristic features of metabolically stressed or “primed” monocytes, a proinflammatory monocyte phenotype associated with metabolic diseases [6,49]. The gene discussed is DUSP1; the disease is metabolic disease.