Previous studies have shown that enhanced ERS and the activation of UPR pathways play a pathogenic role in leptin resistance [44]; later, scholars reported that in non-small-cell lung cancer, leptin down-regulates the protein level of CHOP through the PERK and ATF6 signaling pathways and thus inhibits apoptosis induced by ERS, revealing that ERS plays an important role in the biological effects of leptin [45]. The gene discussed is LEP; the disease is non-small cell lung carcinoma.