For instance, increased palmitoylation of fatty acid translocase CD36 promotes its localization on the plasma membrane of hepatocytes, thus enhancing FA uptake and lipid accumulation, finally contributing to non‐alcoholic steatohepatitis;[12] palmitoylation of myeloid differentiation primary response protein (MYD88), due to de novo FA synthesis, activates the downstream inflammatory signaling in sepsis.[13] Nevertheless, it is still unknown whether or not palmitoylation is involved in cardiovascular dysfunction in response to elevated PA level. This evidence concerns the gene CD36 and metabolic dysfunction-associated steatohepatitis.