One such inhibitor, KH‐3, could disrupt HuR‐FOXQ1 mRNA interactions, hindering breast cancer cell growth and invasion.[46] Furthermore, disrupting lncRNA MAARS‐HuR interactions could reduce macrophage apoptosis and vascular remodeling in advanced plaques across various chronic diseases.[47] Therefore, TUG1‐HuR interactions could be leveraged to develop targeted treatments. The gene discussed is ELAVL1; the disease is breast carcinoma.