Similarly, Katsiki et al. (2024) demonstrated that lean MASLD patients with preserved metabolic profiles experienced hepatic inflammation and fibrosis progression, highlighting that non-traditional mechanisms such as sarcopenia, visceral adiposity, “thin-outside–fat-inside” (TOFI) body composition phenotype, even in the absence of overt obesity, and genetic variants (PNPLA3, TM6SF2) contribute to disease pathogenesis [24]. The gene discussed is PNPLA3; the disease is obesity due to melanocortin 4 receptor deficiency.