SLC9A6 and metabolic dysfunction-associated steatotic liver disease: 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.