Primary liver cancer is the second most frequent cause of cancerārelated deaths. Ferroptosis, a recognized form of regulated cell death, recently gains attention. MicroRNAā214ā3p (miRā214) plays a regulatory role in hepatocarcinogenesis. However, the role of miRā214 in cellular ferroptosis is unclear. This study aimed at elucidating whether miRā214 could regulate ferroptosis of liver cancer. In vitro, HepG2 and Hep3B cancer cells were treated with erastin, a ferroptosis inducer, and then erastin was demonstrated to suppress the cell viability. Moreover, preāmiRā214 overexpression caused that HepG2 and Hep3B cells were more susceptible to erastin, whereas antiāmiRā214 sponge showed the opposite effect. Additionally, preāmiRā214 overexpression increased the malondialdehyde and reactive oxygen species levels, upregulated Fe2+ concentration, and decreased glutathione levels in cancer cells exposed to erastin. Further, erastin enhanced the activation of transcription factor 4 (ATF4) in HepG2 and Hep3B cells, and preāmiRā214 overexpression inhibited ATF4 expression. The luciferase reporter data validated ATF4 as a direct target of miRā214. Cancer cells transfected with ATF4 overexpression plasmid rendered lower susceptible to miRā214āinduced ferroptotic death. In vivo, erastin significantly reduced the size and weight of xenografted tumors, and miRā214 elevated the ferroptosisāpromoting effects of erastin and decreased ATF4 expression. In summary, our study demonstrates that the ferroptosisāpromoting effects of miRā214 in hepatoma cells are attributed at least to its inhibitory effects on ATF4, which may provide a new target for therapy of hepatoma regarding ferroptosis.