Other mechanisms to control ATP/AMP levels involve the tumor suppressor LKB1 and its target the AMP-activated Kinase: loss of function mutations and deletions of LKB1 in non-small cell lung cancers47 and Peutz-Jeghers Syndrome48, and activating mutations in PI3K and AKT that lead to strong signaling increasing glycolytic flux and ATP (and thus preventing the activation of AMPK through high levels of AMP)49, 50, 51. The gene discussed is STK11; the disease is neoplasm.