Despite a mechanistic rationale linking neutrophils and CXCR2 to IR and possibly IR-associated NAFLD [17], to date, there are no studies aimed at short-circuiting only neutrophil function and only neutrophil-driven inflammation in progressive obesity-driven metabolic dysregulation that results in IR and associated liver pathology precipitating NAFLD/NASH. The gene discussed is CXCR2; the disease is metabolic dysfunction-associated steatotic liver disease.