An exploration of the molecular mechanism revealed that circKIAA1797 could bind to the ferredoxin 1 (FDX1) mRNA, reduce FDX1 mRNA stability, inhibit FDX1 expression and bind to the signal transducer and activator of transcription 1 (STAT1) protein and inhibit lipoyltransferase 1 (LIPT1) transcription; moreover, circKIAA1797 could promote the mitochondrial permeability transition pore (mPTP) closure, which in turn inhibited cuproptosis and ultimately promoted the development of lung cancer. The gene discussed is LIPT1; the disease is lung cancer.