Several mechanisms have been proposed to explain malaria tolerance or ‘anti-disease’ immunity [14], [16] including antibody-mediated neutralization of P. falciparum pathogen-associated molecular pattern (PAMP) molecules such as GPI anchors [14], [17], [18]; desensitization of pattern-recognition receptor (PRR)-mediated signaling as a result of repeated stimulation [16]; and the production of anti-inflammatory mediators such as IL-10 [2], [19]–[21] and TGF-β [21]–[23] that suppress inflammation-driven anti-parasite effector mechanisms once parasite replication has been controlled [14]. The gene discussed is TGFB1; the disease is malaria.