Since LPS is also known to bind to Toll-like receptor 4 (TLR4) on the surface of macrophages, promoting their polarization into an M1 phenotype [26,27], we believe our findings link the known aspects of the pathogenesis of bone erosion in cholesteatoma with macrophage polarization in the perimatrix, further establishing acquired cholesteatoma as an inflammatory, immune-mediated disease [57,58,59]. The gene discussed is TLR4; the disease is cholesteatoma.