Engagement of PRRs such as toll-like receptors (TLR), nod-like receptors (NLR) and CLRs, and the downstream immune responses that are elicited is critical for dictating outcomes of individual disease during TB or HIV as previously reviewed (Mesman and Geijtenbeek, 2012; Hossain and Norazmi, 2013; Mortaz et al., 2015). This evidence concerns the gene LARS1 and tuberculosis.