Overactivation of STAT3 could promote tumor growth either directly through tumor autonomic mechanisms or indirectly by modulating antitumor responses.[16] In our study, we observed that C21orf58 accelerated the cell cycle, and enhanced the expression of p‐STAT3 and its target genes (CyclinD1 and IL‐6), which were involved in promoting cell growth.[8b] Besides, the expression of p‐STAT3 and C21orf58 showed a positive correlation in clinical HCC tissues. Here, IL6 is linked to neoplasm.