CD93 signaling inhibition with anti-CD93 mAb led to tumor vessel normalization rather than depletion as evidenced by maturation of blood vessels with increased pericyte coverage via upregulated immunofluorescent staining of alpha-smooth muscle actin (αSMA) and neural/glial antigen 2 (NG2) coverage of vessel structures [14]. The gene discussed is ACTA1; the disease is neoplasm.