Dysfunction of components of this pathway such as hyperactivity of Phosphatidylinositol 3-kinase (PI3K), loss of function of Phosphatase and tensin homolog (PTEN), and gain-of-function of Phosphatidylinositol 3-kinase (AKT), are notorious drivers of treatment resistance and disease progression in cancer (94). This evidence concerns the gene PTEN and cancer.