This is conceivable given reports that M. tuberculosis survival post-therapy may involve infection of CD271(+) bone marrow-mesenchymal stem cells, which may act as a protective intracellular niche for M. tuberculosis persistence, and given that toll-like receptor stimulation of osteoclast precursors inhibit their differentiation into non-inflammatory mature osteoclasts during microbial infection, instead maintaining the phagocytic activity of the precursor cells (Takami et al., 2002). Here, NGFR is linked to infection.