In spite of the evidence linking neutrophils and CXCR2 to T2D and possibly T2D-associated NAFLD [17], to date there are no studies aimed at short-circuiting neutrophil function and neutrophil-driven inflammation independently of macrophages—well known participants in the progression of HFD pathology towards NAFLD/NASH [24–35]—in progressive obesity-driven metabolic dysregulation that results in T2D and associated NAFLD. This evidence concerns the gene CXCR2 and type 2 diabetes mellitus.