Also, ASMTL‐AS1 was explained as a contributor to the malignant phenotypes of both Huh7 and Huh7‐H cells, opposite to the role of lncRNA FUNDC2P4 in residual HCC after insufficient RFA.15 Furthermore, we identified that ASMTL‐AS1 up‐regulation was attributed to the transcriptional activation by MYC, a well‐recognized transcription factor that is always up‐regulated in multiple cancers including HCC.29 This evidence concerns the gene MYC and hepatocellular carcinoma.