Antibody-dependent cellular phagocytosis mediated by macrophages, another proposed alternative mechanism of action, also contributes to antitumor activity of BV in preclinical models.28 Additionally, an analysis of samples from patients with MF and SS found that M2 tumor-associated macrophages can express CD30, suggesting that BV may target these tumor-promoting cells in the tumor microenvironment thus inhibiting their activity.9 CD30-expressing macrophages may internalize BV, releasing the payload MMAE to augment cell death in nearby tumor cells. The gene discussed is TNFRSF8; the disease is synovial sarcoma.