The restoration of mTOR signaling with Fer1 rescue treatment in the context of RSL3 effects, and the genetic knockdown of GPX4, reaffirm our in vitro findings that RSL3-mediated induction of ferroptosis, mTOR pathway suppression, DNA damage and failure of DNA repair, and autophagy are GPX4-dependent processes in thyroid cancer cells. This evidence concerns the gene GPX4 and thyroid gland carcinoma.