Noteworthy, beyond TLR2 and CD36, blockade of CD14 and CD11b/CD18 also inhibited BCG-induced LDs biogenesis and the synthesis of lipid mediators, suggesting that in addition to CD36 other TLR2 co-receptors may regulate mycobacterial infection-triggered alterations in host lipid metabolism (Almeida et al., 2014). This evidence concerns the gene TLR2 and mycobacterial infectious disease.