First, although EBP inhibition likely contributed to the suppressive effects of clemastine, we cannot rule out the potential promiscuity of clemastine and that additional pathways (e.g., histamine/muscarinic receptor signaling) might participate in mediating clemastine’s effects, as suggested by the remaining sensitivity of shEbp mouse glioma cells to clemastine (Figure 4E and Figure S7F). The gene discussed is EBP; the disease is glioma.