While we recognize the need for additional in vivo models to validate our hypothesis, we believe that models currently under development, such as liver organoids derived from patients, could help address questions regarding the expression levels of STARD3 in MASLD patients versus controls, whether patients exhibit a different response to lutein compared to controls, and whether differences in TFEB expression, previously documented in MASLD patients, could also influence the response to lutein treatment. Here, STARD3 is linked to metabolic dysfunction-associated steatotic liver disease.