Preclinical work showed inhibiting PIM3 kinase reverses hypoxia‑induced CAR‑T dysfunction, improving T cell persistence and antitumor activity in solid tumor models. The study identifies PIM3 as a metabolic checkpoint that blunts engineered T cell efficacy in tumor microenvironments characterized by low oxygen, suggesting a pharmacologic strategy to extend CAR‑T utility beyond hematologic cancers. Separately, industry leaders emphasize that scaling CAR‑T and CAR‑Treg therapies requires automation, robust global networks, and platform standardization. Lonza and CDMOs highlight the need for early process development and automation to overcome patient‑specific manufacturing complexity and to reduce per‑dose cost and variability. Why it matters: a dual imperative emerges — actionable biology to make CAR‑T work in solid tumors (PIM3 targeting) and urgent manufacturing innovation to deliver therapies at scale.