The most common metabolic changes occurring in cancer cells are closely intertwined with aberrations in oncogenic and tumor-suppressive pathways that are known to contribute to the expression status of immune checkpoints such as PD-L1 (e.g., Phosphatase and tensin homolog (PTEN)/liver kinase B (LKB) deletions, PI3K/protein kinase B (AKT) mutations, MYC overexpression, signal transducer and activator of transcription 3 (STAT3) activation, etc.)[104,105,106,107]. The gene discussed is AKT1; the disease is neoplasm.