To further confirm the tumor-inhibition effect of TMED2 and whether it was mediated through the TLR4/NF-κB signaling pathway, we used an activator of TLR4 (sparstolonin B) to boost TLR4 expression and observed the changes in the downstream inflammatory factors using western blotting (Fig. 6). The gene discussed is NFKB1; the disease is neoplasm.