Up-regulated programmed cell death protein-1/its ligand 1 expression promotes metabolic dysfunction-associated steatotic liver disease malignant progression.

This editorial focuses on the recent article by Yang in the , which highlights the role of interlukin-17A in promoting hepatocellular carcinoma (HCC) progression by up-regulated programmed cell death protein-1 (PD-1)/programmed cell death protein ligand-1 (PD-L1) expression. Previous, the high PD-1/PD-L1 level was due to hepatitis virus infection leading to systemic innate immune tolerance and cluster of differentiation 8 + T cells exhaustion, ultimately leading to HCC. Recently, interesting studies have found that the malignant progression of metabolic dysfunction-associated steatotic/fatty liver disease (MASLD/MAFLD), that is former nonalcoholic fatty liver disease, was achieved by up-regulated PD-L1 level that was activated the cGAS-STING pathway under lipid accumulation with mitochondrial DNA overflow and up-regulated PD-1/PD-L1 to promote MASLD malignant transformation immune escape. These data suggested that PD-1 or PD-L1 should be a promising target for preventing or delaying non-viral liver disease malignant progression except of antiviral therapy for HCC.