While the presence of other molecules like LAG3 or TIM3 on NExT can improve tumor targeting and accumulation, our focus remained on PD1 due to its consistent retention on NExT (Fig. 2c-e), identifying PD1/PDL1 interaction as a primary mechanism for specific targeting and intratumor accumulation, and supporting the relevance of PD1/PDL1 interaction for NExT specificity in targeting PDL1+ tumors (Fig. 3), as observed in prior studies with other platforms [56, 57]. The gene discussed is HAVCR2; the disease is neoplasm.