Excess glucose engages canonical insulin signaling [insulin receptor substrate (IRS)—phosphoinositide 3-kinase (PI3K)—protein kinase B (Akt)] to drive glucose transporter type 4 (GLUT4) translocation in skeletal muscle and adipose tissue; impaired signaling delays vesicle delivery and prolongs hyperglycemia (26). This evidence concerns the gene SLC2A4 and Hyperglycemia.