Despite the differences, the MyD88-dependancy of both ply+lytA+ bacteria and Δ(lytA’-ply’)593-induced TNFα responses highlights that MyD88 is a critical signalling hub in the protective response to S. pneumoniae, as demonstrated by the recurrent and severe pneumococcal infections in young people with genetic MyD88 deficiency [70]. The gene discussed is TNF; the disease is pneumococcal infection.