We found that treatment with the proteasomal inhibitor MG132 inhibited the decrease in PD‐1 protein levels caused by PTBP3 knockdown, implicating the proteasomal degradation pathway (Figure 4B; Figure S4F, Supporting Information).[35] It has been reported that FBXO38 mediates PD‐1 ubiquitination and regulates the anti‐tumor function of T cells.[36] Interestingly, PTBP3 knockdown significantly upregulated FBXO38 at both the RNA and protein levels (Figure 4C,D). The gene discussed is PTBP3; the disease is neoplasm.