To target this pathway for the treatment of hyperglycemia in T1D, whereas the available compounds used for other diseases were not effective in reducing glucagon hypersecretion from either mouse or human islets (Supplemental Figure 1, A–E), we showed a direct interaction between WCDD301 and the EphA4 receptor in vitro (Figure 1, B–E) and that this interaction recapitulates the action of soluble Ephrin-A5 in both isolated islets and dispersed islet cells. The gene discussed is EFNA5; the disease is Hyperglycemia.