16 31 32 While previous studies have shown that SQLE promotes tumor progression and suppresses antitumor immunity in steatosis-driven HCC models, our study demonstrates that SQLE also impairs CD8+ T cell function in non-steatotic HCC.16 33 Specifically, SQLE inhibition enhanced CD8+ T cell activation without altering cholesterol levels in the tumor-conditioned medium, suggesting an alternative mechanism involving oxysterol-mediated cholesterol restriction. Here, CD8A is linked to steatosis.