When aberrant activation of upstream mutated tyrosine kinase receptors (TKRs) and RAS, as well as, functional loss of the tumour suppressor gene PTEN (phosphatase and tensin homolog) and INPP4B (type II inositol polyphosphate-4-phosphatase) occur, the PI3K/AKT/mTOR pathway becomes constitutively activated—A hallmark of many cancers, including pancreatic [136]. This evidence concerns the gene INPP4B and cancer.