These findings closely followed another major revelation that the tumor suppressor LKB1 (Liver Kinase B1; also known as Serine/Threonine Kinase 11 – STK11) is a direct activator of AMPK (Hawley et al., 2003; Hong et al., 2003; Shaw et al., 2004; Woods et al., 2003), and that polarity defects precede the development of tumors in genetically modified mice with tissue-specific deletion of LKB1 (Hezel et al., 2008). Here, PRKAA2 is linked to neoplasm.