Targeting glutamine utilization as an anti-cancer strategy shows promise for those tumor types which exhibit “glutamine addiction,” often associated with specific genomic alterations such as c-myc upregulation, KRAS mutations, mTOR upregulation, and NRF2 activation, as well as loss of tumor suppressors such as PTEN and RB1 [10]. The gene discussed is PTEN; the disease is neoplasm.