Interaction of PI(3,4)P2 with the pleckstrin homology (PH) domain of AKT is required for dimerization and full activation of AKT,8 so like phosphatase and tensin homolog (PTEN), INPP4B may act as a tumour suppressor by antagonizing the PI3K/AKT signalling pathway.9 However, recent reports demonstrated the controversial role of INPP4B in carcinogenesis in various tumours. This evidence concerns the gene PLEK and neoplasm.