Critically, the tumor-suppressive phenotypes induced by UNC93B1 knockdown, including the inhibition of proliferation, migration, and clonogenicity, were largely reversed upon treatment with the selective STING inhibitor H-151, confirming that the observed functional consequences are causally mediated through the activation of the cGAS-STING pathway.<h4>Conclusion</h4>By integrating multi-omics data, including GWAS and spatial transcriptomics, this study systematically defines a pivotal role for UNC93B1 in PDAC progression. Here, STING1 is linked to neoplasm.