TAF15, also known as TATA-binding protein-associated factor 2N, is a DNA and RNA binding protein. It is involved in crucial inflammatory signalling pathways and is a member of the FUS-Ewing sarcoma-TAF15 family. TAF15 may play roles in processes like lipid metabolism, inflammation regulation, and cell-cycle-related events, and its misfolding might be linked to neurodegenerative diseases [1,2,5].

In non-alcoholic steatohepatitis (NASH), hepatocyte-specific knockdown of TAF15 using an adeno-associated virus inhibited steatosis, inflammation, and fibrosis, while overexpression promoted NASH phenotypes. TAF15 bound to the promoter region of FASN to facilitate its expression and interacted with p65 to activate the NF-κB signalling pathway [2]. In gastric cancer, TAF15 knockdown suppressed cell proliferation, migration, and invasion in vitro and inhibited tumour growth in vivo, with reduced phosphorylation levels of RAF1, MEK, and ERK1/2 [3]. In osteoarthritis, knockdown of TAF15 suppressed chondrocyte apoptosis and ECM degradation in vivo and cartilage pathological changes in vitro [4].

In conclusion, TAF15 plays important roles in multiple disease conditions such as NASH, gastric cancer, and osteoarthritis. Studies using knockdown models in these diseases have revealed its functions in regulating lipid metabolism, inflammation, cell proliferation, and tissue-specific pathological changes, providing insights into potential therapeutic targets for these diseases.