DDR1 and neoplasm: These findings suggest that DDR1 mutation or expression may not be the primary drivers of its oncogenic activity in NSCLC and that DDR1-driven tumor progression may rely more on microenvironmental interactions (e.g., ECM remodeling) rather than intrinsic genomic instability, with DDR1 overexpression promoting collagen alignment and creating a barrier to immune infiltration independent of mutational burden (10).