Inhibition of USP7 with small molecules such as P5091 — which primarily targets USP7 rather than USP22 directly — promotes PD-L1 degradation and enhances responsiveness to PD-1 blockade, and may also indirectly affect USP22-mediated pathways to disrupt cancer stemness programs by downregulating transcription factors such as SOX2 and NANOG([42]– [43]). This evidence concerns the gene USP22 and cancer.