Targeting tumor‐specific metabolic vulnerabilities—such as GLUT1, glutaminase (GLS), FASN, or immunosuppressive metabolites—offers a promising strategy to remodel the TME and restore antitumor immunity.[176] However, due to overlapping metabolic dependencies between tumor and immune cells,[17] the development of selective delivery systems (e.g., nanoparticle‐based platforms) and rational combination therapies is essential. The gene discussed is GLS; the disease is neoplasm.