These data suggest that cancer cell-derived CD30EVs but not monomeric sCD30 enable the binding of the anti-CD30 ADC to CD30− but CD30L+ cells, in vitro. Together, these data support the hypothesis that CD30+ EVs from cancer cells allow the off-target binding of SGN-35 to bystander cells of the tumor microenvironment. This evidence concerns the gene TNFSF8 and cancer.