To evaluate whether the pro‐tumorigenic effect of aHSCs depend on FAO, we inhibited FAO in HCC cells treated trimetazidine dihydrochloride (TMZ, 10 × 10−6m).[12] Our results showed that even treating aHSCs with TA9, the restored expression of CPT1A, cellular viability, and ATP production in HCC cells were all reduced again when FAO was inhibited (Figure 2I–K and Figure S8A, Supporting Information). This evidence concerns the gene CPT1A and hepatocellular carcinoma.