Through selective targeting to CD30 antigen, a hallmark of HL and ALCL, brentuximab vedotin is internalized via a clathrin‐dependent mechanism and transferred into endosomes and lysosomes where the linker is hydrolyzed by cysteine proteases, like cathepsin B. The released free MMAE then targets to tubulin to inhibit its polymerization, causing cell cycle arrest and cell apoptosis.132 In virtue of bystander effects, brentuximab vedotin is able to take effect for those antigen-negative cancer cells. This evidence concerns the gene CTSB and Hodgkins lymphoma.