Characteristics of cancer metabolism, such as increased metabolic flux through intermediary metabolism to sustain proliferation, are primarily a consequence of alterations in signal transduction networks, such as PI3K-AKT-mTORC1, rather than direct mutations in metabolic enzymes.33,71 Given the broad range of targets in metabolic cancer therapy, there is a critical need to identify biomarkers that predict metabolically sensitizing alterations, facilitating patient stratification for targeting metabolic pathways in parallel with SoC treatments within a personalized medicine framework.39 This evidence concerns the gene PIK3CA and cancer.