Altogether, the upregulation of Fabp7 in GFAPTg;Gfap+/R236H mice and FABP7 in AxD patients is expected to induce a harmful phenotype by generating an NF-κB inflammatory response (78) resulting in heightened levels of Gfap (79) and decreasing the anti-inflammatory effects of the PPAR pathway (80, 81). Here, GFAP is linked to Alexander disease.