Moreover, cholesterol interacts directly with the transmembrane domain of PD‐L1, facilitating immune evasion by forming a sandwich‐like structure that stabilizes PD‐L1 and protects it from ubiquitination‐mediated proteasomal degradation in cancer cells.[30] We hypothesized that silencing piRNA‐137463 might downregulate the expression of PD‐L1 by promoting its proteasomal degradation. This evidence concerns the gene CD274 and cancer.