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. Here, HMG20A is linked to Alzheimer disease.