Besides the role in brain edema, we have previously demonstrated that the aggregation state of AQP4, ranging from tetramers to different sized OAPs, can influence glioma cell fate as follows: AQP4-OAP expression leads to cell shrinkage with alteration in the actin cytoskeleton and apoptotic outcome being therefore "deleterious" for glioma cell survival, while AQP4-tetramer expression increases glioma invasive capability being therefore "beneficial" for glioma cells [17]. The gene discussed is AQP4; the disease is glioma.