In KPC mice, the inhibition of focal adhesion kinase (FAK) also reduces tumour fibrosis and immunosuppressive cell infiltration (MDSCs, tumour‐associated macrophages and Tregs) resulting in enhanced response to checkpoint blockade (anti‐PD1 and anti‐CTLA4) and chemotherapy [22]; in this model, tumour‐cell intrinsic FAK appears to be the key driver of CAF expansion, tumour fibrosis, and immune suppression, in contrast to the previously described CAF intrinsic mechanisms. Here, CTLA4 is linked to neoplasm.