FCGRT and chronic inflammatory demyelinating polyradiculoneuropathy: Although the primary mechanism of efgartigimod is the depletion of circulating IgG via FcRn blockade, its clinical efficacy in CIDP—where no specific target antibody has been defined—suggests that indirect downstream effects, such as reduced immune complex-mediated complement activation or modulation of proinflammatory cytokine pathways, may contribute to its therapeutic action.