In both Crohn’s disease and ulcerative colitis, or UC, inflammation can keep coming back like relentless weeds. IL-23, an inflammatory cytokine, is one of the known drivers of inflammation in Crohn’s disease and UC. Blocking IL-23 after it is produced can limit inflammation. But what if it were possible to block IL-23 inflammation at its cellular source? CD64-positive immune cells are the main producers, and the root source, of IL-23. TREMFYA^® (guselkumab) is the only dual-acting IL-23 inhibitor. TREMFYA^® works by BLOCKING IL-23, a cytokine responsible for inflammation, and BINDING to CD64, a receptor on cells that produce IL-23. The clinical significance of these findings is unknown. TREMFYA^® is an IL-23 blocker indicated for the treatment of adult patients with moderately to severely active Crohn’s disease or moderately to severely active UC. Similar to other IL-23 inhibitors, TREMFYA^® binds to the p19 subunit of IL-23 and inhibits its interaction with the IL-23 receptor, thereby inhibiting the release of pro-inflammatory cytokines and chemokines. Unlike other IL-23 inhibitors, only TREMFYA^® is designed with a dual-acting structure that blocks IL-23 and also binds to CD64, a receptor on cells that produce IL-23. Binding to CD64 positions TREMFYA^® to block IL-23 at its cellular source, allowing it to work at the root of IL-23–driven inflammation. TREMFYA^®: the only dual-acting IL-23 inhibitor that neutralizes inflammation at its cellular source. Based on in vitro studies in an inflammatory monocyte model. The clinical significance of these findings is unknown.