We hypothesize that the hosts adopt an “active killing” strategy at the early stage of infection, which involves the aggregation of immune cells such as Spp1+ MoMFs and neutrophils to kill the parasite, and then change into a “negative segregation” strategy at the middle and late stage of infection, which involves fibrosis formation surrounding the E. multilocularis microcysts trying to contain pathogen growth (Figure7). The gene discussed is SPP1; the disease is infection.