While it is likely that in many tumors only low numbers of dendritic cells and neutrophils directly interact with the PDPN CAFs, new immunotherapies that engender more immune infiltration could shift the balance and lead to enough CLEC-2/CD177 in the tumor stroma to collectively inhibit PDPN and the pro-tumor CAF functions. The gene discussed is CLEC1B; the disease is neoplasm.