The rationale here is to block with the anti-PD-1 mAb the binding of PD-L1 (present on the tumor cells) to its receptor PD-1 (present on T cells), avoiding the suppression of antitumor responses triggered by the PD-L1/PD-1 interaction, while targeting mesothelin+ cells with the BMS-986148 mAb. Here, CD274 is linked to neoplasm.