Furthermore, PAFR antagonist could reduce SP-mediated PI3K/AKT, NF-kB, and cell proliferation in the lung cancer animal model, further supporting that the PspC and PAFR interaction is essential for the tumor-promoting effect of SP. Therefore, SP infection could play an oncogenic role in lung carcinogenesis by activating PI3K/AKT and NF-kB oncogenic pathways via binding PspC to PAFR. The gene discussed is NFKB1; the disease is neoplasm.