The pathogenesis of MASLD involves complex metabolic, inflammatory, and cellular stress processes.24 Hepatic fat accumulation activates the immune system, leading to leukocyte aggregation and the production of inflammatory cytokines such as tumor necrosis factor-α and interleukin (IL)-6.25 These cytokines stimulate the liver to produce more CRP, thereby elevating hs-CRP levels. Here, CRP is linked to metabolic dysfunction-associated steatotic liver disease.