We could demonstrate, that in addition to other molecular pathways leading to phenotypic and functional cellular change, AHNAK2 protein expression was increased in hypoxia with an increase co-localisation in cellular process along with Cortactin, contributing to the mesenchymal phenotype, at least in some of cancer cell lines where there was cytoplasmic and not vesicular distribution of AHNAK2 during normoxia. This evidence concerns the gene AHNAK2 and cancer.