Collectively, these findings support a working AOP model linking DEHP-responsive KLF5-centered activity to extracellular matrix (ECM) remodeling and immunomodulatory communication, providing a mechanistic rationale that aligns with signaling programs characteristic of therapy-tolerant tumor niches, particularly PI3K-AKT-coupled survival signaling and TGF-β-linked stromal remodeling. The gene discussed is KLF5; the disease is neoplasm.