Cancer immunotherapy has emerged as the fourth most prevalent approach to tumor treatment, alongside surgery, radiotherapy, and chemotherapy. After several decades of development, chimeric antigen receptor T (CAR‐T) cell therapy, a promising branch of adoptive T‐cell therapy, has demonstrated superior efficacy and safety in comparison to other cell therapies in the treatment of cancer. At present, CAR‐T cells are predominantly used to treat hematological malignancies, although their application in solid tumors is being readily investigated. Although numerous studies have examined the biomarkers associated with the safety of CAR‐T cell therapy, few have evaluated predictors of CAR‐T cell therapeutic efficacy. Thus, the primary objective of this review article was to provide a comprehensive overview of the factors predicting the efficacy of CAR‐T cell therapy, with a particular focus on biomarkers and their detection methods.

Non-alcoholic steatohepatitis (NASH), a progressive form of non-alcoholic fatty liver disease (NAFLD), is characterised by chronic liver inflammation, which can further progress into complications such as liver cirrhosis and NASH-associated hepatocellular carcinoma (HCC) and therefore has become a growing health problem worldwide. The type Ⅰ interferon (IFN) signaling pathway plays a pivotal role in chronic inflammation; however, the molecular mechanisms underlying NAFLD/NASH from the perspective of innate immune response has not yet been fully explored. In this study, we elucidated the mechanisms of how innate immune response modulates NAFLD/NASH pathogenesis, and demonstrated that hepatocyte nuclear factor-1alpha (HNF1A) was suppressed and the type Ⅰ IFN production pathway was activated in liver tissues of patients with NAFLD/NASH. Further experiments suggested that HNF1A negatively regulates the TBK1-IRF3 signaling pathway by promoting autophagic degradation of phosphorylated-TBK1, which constrains IFN production, thereby inhibiting the activation of type Ⅰ IFN signaling. Mechanistically, HNF1A interacts with the phagophore membrane protein LC3 through its LIR-docking sites, and mutations of LIRs (LIR2, LIR3, LIR4, and LIRs) block the HNF1A-LC3 interaction. In addition, HNF1A was identified not only as a novel autophagic cargo receptor but also to specifically induce K33-linked ubiquitin chains on TBK1 at Lys670, thereby resulting in autophagic degradation of TBK1. Collectively, our study illustrates the crucial function of the HNF1A-TBK1 signaling axis in NAFLD/NASH pathogenesis via cross-talk between autophagy and innate immunity.