Gap junctions are specific cell-to-cell channels formed by membrane proteins called connexins (Cx). Connexin43 (Cx43) is the major connexin expressed in human microvascular endothelial cells (HMEC), astrocytes and glioblastoma cells. Cx43 is specifically upregulated in the reactive astrocytes surrounding glioblastoma , suggesting that gap junctions at the tumor margins are involved in tumor cell invasion [4, 6, 8, 9] and tumor growth . The precise role of gap junctions remains poorly understood. Nevertheless, microRNAs (miRs) were observed to be exchanged between glioblastoma cells  and normal astrocytes  through gap junctions. MiRs are small non-coding RNAs that modulate gene expression by affecting the translation of messenger RNAs (mRNAs) into proteins and inducing target mRNA decay [12–14]. A miR is single-stranded and ~21nucleotides long, forming a linear molecule with a diameter of ~1.0 nm, which is in the same order of the gap junction channel pore size [15, 16]. We have recently reported that miR-145-5p, which reduces glioma growth , could be exchanged between HMEC and colon cancer cells through gap junctions formed by Cx43 .