Furthermore, clinical studies on lung adenocarcinoma have shown that LINE-1 forms a chimeric transcript LCT (L1-FGGY) with the tumor suppressor gene FGGY via reverse transcriptional translocation, and analysis of its function suggests that LCT deletion activates the arachidonic acid (AA) metabolic pathway and promotes tumor growth, which can be effectively targeted by the combination of anti-HIV drugs (NVR) and metabolic inhibitors (ML355) (79). The gene discussed is FGGY; the disease is lung adenocarcinoma.