In conclusion, we provide the evidence that the tumor-promoting properties of ENO1 can be transferred between HCC cells with high/low ENO1 expression via exosome-mediated crosstalk, promoting the growth and metastasis of HCC by upregulating integrin α6β4 expression and activating the FAK/Src-p38MAPK pathway (Fig. 7). Here, SRC is linked to neoplasm.