The results revealed that compared to ΔAmoG infection, CCL1 and ΔAmoG-C infection notably repressed the expression of several key genes, including wnt10b, axin2, ccnd1, and ctnnb1, whereas genes like IL-8, ptx3a, and hsp90b1 experienced pronounced upregulation (Figure 3A,B). The gene discussed is CTNNB1; the disease is infection.