Function analysis of a tumor specific and frequent LCT involving FGGY (L1-FGGY) reveal that the AA metabolic pathway was activated by the loss of FGGY through the L1-FGGY chimeric transcript to promote tumor growth, which was effectively targeted by a combined use of an anti-HIV drug (NVR) and a metabolic inhibitor (ML355). The gene discussed is FGGY; the disease is neoplasm.