In contrast, therapy with the humanized anti-CD30 brentuximab-vedotin antibody, that acts via a potent antimitotic agent (auristatin E) emerged as a potential candidate therapy for SM due to its ability (i) to induce apoptosis on neoplastic MC, (ii) to down-regulate of IgE-mediated histamine release, and (iii) to synergize with midostaurin to inhibit neoplastic MC growth in vitro [79]. This evidence concerns the gene TNFRSF8 and systemic mastocytosis.