The recent work by Shengir et al. offers compelling insight into the evolving metabolic landscape following hepatitis C virus (HCV) eradication via direct-acting antivirals (DAAs). While liver stiffness and fibrosis indices significantly improved post-SVR, hepatic steatosis (HS) paradoxically increased in prevalence, highlighting a shift from virus-driven injury to metabolic dysfunction-associated steatotic liver disease (MASLD). In this correspondence, we expand upon these findings by discussing the clinical and pathophysiological implications of post-SVR steatosis, underscoring the need for ongoing metabolic surveillance even in patients with virologic cure. We also emphasize the limitations of traditional risk stratification based on BMI alone and call for refined, longitudinal approaches to detect and manage metabolic liver disease in the post-SVR population.