Taken together, our findings provide a molecular basis for the spatial translocation of SLC9A6‐126aa in response to high‐fat stress and identify SLC9A6‐126aa as a novel AKT1 downstream substrate that contributes to lipid dyshomeostasis in NAFLD through escape from the phosphorylation of AKT1. Here, AKT1 is linked to metabolic dysfunction-associated steatotic liver disease.