Moreover, PD-L1 overexpression resulting from either PKP3 overexpression or circIGF2BP3 overexpression was sufficient to impair anti-PD-1 treatment-mediated activated CD8+ T cell recruitment and tumor regression, also confirming the fact that circIGF2BP3/PKP3-mediated PD-L1 upregulation plays the main role in regulating anti-PD-1 responsiveness (Fig. S8E-G). Here, PKP3 is linked to neoplasm.