<b>Conclusions:</b> These findings uncover a critical mechanism by which tumor cells counteract ferroptosis by WTAP-mediated <i>GLS</i> alternative splicing under EGFR activation, highlighting the therapeutic potential of targeting the m<sup>6</sup>A-dependent GLS isoform switch in HCC and offering a rationale for the development of combination therapies. The gene discussed is GLS; the disease is hepatocellular carcinoma.