HMG20A and myeloid sarcoma: This molecular model could rationalize our findings that obese non-diabetic individuals have higher levels of HMG20A in WAT favoring an anti-inflammatory and pro-survival cell phenotype whereas obese diabetic patients expressed normal levels of HMG20A indicative of a non-reactive cell phenotype incapable of relaying cell protection and repair ultimately leading to neurodegeneration disease such as MS or AD as well as other complications such as altered glucose homeostasis.