For instance, enzalutamide resistance emerges via SE‐driven CHPT1 overexpression in CRPC, regulated by AR binding to distinct enhancers and lncRNA‐mediated H3K27ac reader BRD4 interaction, highlighting SE‐targeted CHPT1 inhibition as a therapeutic strategy to overcome enzalutamide resistance.[27] Additionally, mounting evidence suggests that inhibiting SE‐driven genes is a viable anti‐cancer strategy. The gene discussed is CHPT1; the disease is cancer.