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. This evidence concerns the gene STAT1 and lung carcinoma.