FBXL5 has been identified as a downstream effector of ALKBH5, whose ablation was previously reported to alleviate iron overload in cancer cells, leading to a rise in oxidative stress and, as a result, compensatory proliferation in cancer cells.[16] Therefore, conversely, we hypothesized that ALKBH5‐FBXL5 exerted tumor suppressive function via ROS reduction. This evidence concerns the gene ALKBH5 and neoplasm.