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Researchers from the Olivia Newton‐John Cancer Research Institute and the La Trobe University School of Cancer Medicine have found a novel drug target to potentially improve the treatment of pancreatic cancer. Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with a low 5‐year survival rate and is associated with poor response to therapy. Elevated expression of the myeloid‐specific haematopoietic cell kinase (HCK) is observed in PDAC and correlates with reduced patient survival. To determine whether aberrant HCK signaling in myeloid cells is involved in PDAC growth and metastasis, the researchers established orthotopic and intrasplenic PDAC tumors in wild‐type and HCK knockout mice. Genetic ablation of HCK impaired PDAC growth and metastasis by inducing an immune‐stimulatory endotype in myeloid cells, which in turn reduced the desmoplastic microenvironment and enhanced cytotoxic effector cell infiltration. Consequently, genetic ablation or therapeutic inhibition of HCK minimised metastatic spread, enhanced the efficacy of chemotherapy, and overcame resistance to anti‐PD1, anti‐CTLA4, and stimulatory anti‐CD40 immunotherapy. The researchers argued their results provided a strong rationale for HCK to be developed as a therapeutic target to improve the response of PDAC to chemo‐ and immunotherapy. The study was published in Cell Reports. “This is important because most pancreatic cancer patients do not respond to existing anti‐cancer drugs, and the survival rate of pancreatic cancer has not improved over the past few decades. We hope to eventually translate these findings into the clinic and improve survival outcomes for pancreatic cancer patients,” lead author Dr Ashleigh Poh said.