Adeno‑associated virus (AAV) vectors offer safety and durable expression but lack tumor specificity. This hypothesis proposes an NSCLC‑directed, hypoxia‑responsive AAV platform that integrates MGS4 peptide‑guided capsid targeting with dual hypoxia‑responsive element (HRE)‑gated promoters driving Q‑CXCL9‑Fc (chemokine) and miR‑30‑based shRNA against mesothelin (MSLN).