Similarly, mutations in phosphate and tensin homolog (PTEN)—which occur in 40–60% of melanomas—lead to persistent Akt activation, upregulating glucose uptake and consumption through increased expression of glucose transporter type 1 (GLUT1), hexokinase 2 (HK2), phosphofructokinase 1 (PFK-1) and lactate dehydrogenase A (LDH-A) [24]. This evidence concerns the gene PFKM and melanoma.