Two translational studies identified metabolic vulnerabilities that could be exploited therapeutically. Ding, Zhang, and Huang reported in the Journal of Translational Medicine that glutamine metabolism reprogramming via PYCR1 promotes bladder cancer progression, implicating PYCR1 as a potential metabolic target. Targeting glutamine pathways may disrupt tumor bioenergetics and biosynthesis in aggressive bladder tumors. Separately, a Molecular Diversity report identified a small‑molecule derivative (DAA) that activates autophagy and suppresses non‑small cell lung cancer growth in preclinical models. The compound, derived from an endophyte library, appears to trigger autophagic flux that limits tumor survival. Both papers point to complementary strategies—blocking key metabolic enzymes or enhancing catabolic autophagy—to undermine tumor fitness and provide new leads for drug development in solid malignancies.