Consistently, the knockdown of AKR1B1 significantly decreased SLC7A11 expression, whilst the overexpression of SLC7A11 counteracted ferroptosis and restored cell proliferation and invasion, confirming the AKR1B1–STAT3–SLC7A11 axis as a key pathway in gastric cancer progression, independently of AKR1B1’s enzymatic activity, reinforcing its role as a signaling scaffold in cancer [50]. This evidence concerns the gene SLC7A11 and cancer.