The blockade of Mincle/Syk/NF-κB signaling can repress the TAM-driven NSCLC progression in vivo.284 A recent study demonstrated that CRIP1 facilitated MDSC trafficking and fostered an immunosuppressive TME via facilitating NF-κB/p65 nuclear translocation in pancreatic ductal adenocarcinoma (PDAC), and inhibiting CRIP1/NF-κB/CXCL axis can sensitize PDAC to immunotherapy.243. The gene discussed is CRIP1; the disease is pancreatic ductal adenocarcinoma.