While DNL contributes to hepatic steatosis, it also is linked to very low-density lipoprotein (VLDL) production via ChREBP activation of microsomal triglyceride transfer protein (MTTP) and TM6SF2. Several studies have described an increase in VLDL particle size and number due to increased ChREBP and SREBP1 activity, which was observed due to pharmacological activation of the nuclear receptor LXR, a known regulator of DNL (29, 30). Here, TM6SF2 is linked to fatty liver disease.