Notably, Gunderson et al. found that in pancreas ductal adenocarcinoma-bearing mice, treatment with ibrutinib reprogrammed macrophages toward a Th1 phenotype, which stimulated cluster of differentiation 8-positive (CD8+) T-cell cytotoxicity and decreased tumor development, demonstrating that BTK signaling drives tumor immunosuppression. Here, CD8A is linked to neoplasm.