Given the critical role of ROS formation and regulation in MASLD, it is plausible that the reduced presence of estrogens in postmenopausal women—and the subsequent decrease in estrogen-dependent, TRX2-mediated ROS scavenging—contributes to the more marked decline in TXN2 expression observed in this cohort as the disease progresses. This evidence concerns the gene TXN2 and metabolic dysfunction-associated steatotic liver disease.