At the disease level, dysregulated m1A machinery is linked to malignant phenotypes: overexpression of the TRMT6/TRMT61A writer complex correlates with poor prognosis and supports proliferation and stress tolerance in multiple models (glioma, bladder cancer, hepatocellular carcinoma), while the m1A demethylase ALKBH3 promotes cancer cell growth, invasion, and—in several reports—therapy resistance (33). The gene discussed is ALKBH3; the disease is cancer.