Consistent with the conclusions from in vitro assays, the overexpression of exosomal circCMTM3 could trigger upregulation of p-STAT5A and the downregulation of p-STAT5B, leading to the amplification of CHI3L2 and SRSF1, which, in turn, promoted GBM progression characterized by the level of Ki-67 positivity. The gene discussed is STAT5A; the disease is glioblastoma.