The fast-growing mycobacteria, M. abscessus and M. fortuitum, induced the production of TGF-β at the same levels as in M. tuberculosis; but for infections with the fast growers, TGF-β production was not enough to prevent cell damage induced by a strong proinflammatory response (as has been demonstrated to occur in M. tuberculosis infections). M. celatum induced the highest levels of TGF-β, which could reduce the innate immune response and favour the persistence of this mycobacterium in the host, despite the proinflammatory response mediated by IL-8 secretion. The gene discussed is TGFB1; the disease is infection.