We read with great interest the article by Di Ciaula et al. exploring the association between long-term PM10 exposure and metabolic dysfunction-associated steatotic liver disease (MASLD) in cardiometabolic patients with different genetic risk profiles [1]. By integrating environmental exposure data, genotyping, and dietary assessment, the authors provide biologically plausible evidence supporting a gene–environment interaction in hepatic fat accumulation. The topic is timely and of clear clinical relevance.
