Activate selected toll-like receptors (TLR) in monocytic cells to generate a tolerogenic immune program, TLR2 and TLR5 ligation was demonstrated to induce innate and adaptive immune suppression to promote PDA (Pushalkar et al., 2018); the activation of the mannose-binding lectin–C3 cascade through the C3 complement pathway might cause inflammation induced by the oncogenic Kras, leading to fungal dysbiosis and promoting tumor progression (Aykut et al., 2019). The gene discussed is C3; the disease is Patent ductus arteriosus.