For instance, sulfasalazine exerts a tumor‐suppressive role by inducing ferroptosis, primarily through the upregulation of the iron importer TFRC, and this effect is negatively correlated with estrogen receptor (ER) expression levels in cancer cells.[39] Also, one of the novel transcriptional targets of ER, membrane‐bound O‐acyltransferase domain‐containing 2 (MBOAT2), suppresses ferroptosis by modulating the phospholipid peroxidation process.[40] Our study supports these findings and underscores the need to elucidate how estrogen signaling modulates ferroptosis in the SG. The gene discussed is ESR1; the disease is neoplasm.