Zhang et al (2019) reported that TAMs help tumor cells avoid complement-mediated cell death, providing mechanistic insight into TAM and complement component cross-talk in pancreatic cancer (Zhang et al, 2019). Our data provide evidence for up-regulation of the complement components C1QA and C1QB in PDA TAMs systemically. Further work is needed to determine if the up-regulation of complement components is a side effect of the systemic inflammation caused by PDA or if it is functionally contributing to carcinogenesis (Bettac et al, 2017). The gene discussed is C1QA; the disease is pancreatic neoplasm.