Although a T-cell inflamed preclinical model demonstrated PI3Kδ inhibition together with PD-L1 blockade resulted in enhanced antitumor efficacy (18), studies with the MC38-OVA (murine colon adenocarcinoma) tumor model suggested that PI3Kδ inactivation (kinase-dead PI3KδD910A) negated the antitumor effects achieved with anti-PD-L1 (or anti-CTLA-4) in wild-type mice (29). This evidence concerns the gene CTLA4 and colon adenocarcinoma.