Its overexpression promotes tumor progression by remodeling the ECM and activating the focal adhesion kinase signaling pathway via DDR2, enhancing cancer cell migration and survival.[23] Although direct links to COPD are limited, similar ECM remodeling in both diseases suggests COL10A1 may contribute to a pro-tumorigenic microenvironment in COPD. Here, COL10A1 is linked to neoplasm.