RAS is frequently mutated in CRC and activates several downstream effectors.23 The most intensive studied pathways are RAF/MAPK and PI3K/AKT,23 which are often concurrently activated in many cancers and inhibiting GSK3 by phosphorylating the same residue.24, 25 Immunoblot analysis showed that phosphorylation of AKT, ERK and GSK3β were increased in AQP9-overexpressing CRC cells (Figure 5c). This evidence concerns the gene GSK3B and cancer.