Fibroblast growth factor 4 (FGF4), acting via the PI3K/Akt signaling pathway, also shifts macrophage polarization toward the M2 phenotype, significantly reducing inflammatory damage in ConA-induced hepatitis models; notably, this protective effect is lost upon macrophage depletion, underscoring the specificity of macrophage-mediated responses [16]. The gene discussed is FGF4; the disease is hepatitis A virus infection.