PI4KB and neoplasm: To further validate the therapeutic potential of inhibiting PI4KB phosphorylation on S256 and T263, we lastly utilized a KPC mice model of pancreatic cancer, known for faithfully recapitulating human pancreatic cancer biology.88–90 Consistent with our findings in cancer cell lines and xenograft experiments, treatment with PI4KB-Peptide-1 blocked PI4KB phosphorylation on S256 and T263, and RINCAA in cancer tissues and, in combination with trametinib, effectively suppressed tumor growth and prolonged survival (Fig.10a–f).