Concurrently, enhanced intrahepatic retention of activated NKT cells and CD8+ T cells has been observed to mitigate glucose intolerance, liver steatosis, the release of inflammatory factors (such as IL-10), and tumor growth (via the IRF1/CXCL10/CXCR3 axis) in MASH, consequently suppressing the development of HCC (115–117). Here, CXCL10 is linked to metabolic dysfunction-associated steatohepatitis.