Collectively, our findings indicate that STOML2 facilitates the recruitment of TRADD and sustains NF-κB activity to upregulate CCND1, VEGFC and PD-L1, which consequently leads to tumor proliferation, angiogenesis, immune escape and poorer clinical outcomes in human in CRC (Fig. 7d). This evidence concerns the gene NFKB1 and colorectal carcinoma.