previously discovered to be responsible for ubiquitinating and subsequently degrading MLKL, and they believed that Skp2 partially contributes to the development of cisplatin resistance in non‐small cell lung cancer (NSCLC) cells.[112] The authors also reported that the Skp2 inhibitor SZL P1‐41 can disrupt the Skp2‐related binding and degradation of MLKL in A549 cells.[112] However, the A549 cell line, as a human NSCLC cell line, is not susceptible to necroptosis stimulation. This evidence concerns the gene MLKL and lung cancer.