In TNBC cell models, <i>in vitro</i> experiments supported that miR-148b-3p negatively regulated SLC7A11, and higher SLC7A11 expression was associated with increased glutathione levels, reduced lipid peroxidation, and enhanced cell survival under ferroptosis-inducing conditions.<h4>Conclusions</h4>Our pan-cancer analyses reveal a potential biological link between SLC7A11, ferroptosis, and tumor immunity, generating the hypothesis that SLC7A11 may serve as a biomarker for immune checkpoint inhibitor response. This evidence concerns the gene SLC7A11 and neoplasm.