SEMA3C and neoplasm: Research has shown that HSCs were the main source of CAFs in the TME, and CAFs could cross-talk with tumor cells to influence tumor progression in a paracrine way.7 Thus, we wondered whether Sema3C-induced CAFs activation could in turn regulate Sema3C expression in HCC cells to promote stemness maintenance, thereby creating a vicious cycle between stromal cells and tumor cells.