The survival of Mtb, depends on its ability to invade the host, replicate, and transmit infection. At its initial peripheral infection Mtb infects macrophages, and part of the immune evasion is accomplished by using cell-surface-associated phthiocerol dimycoceroserate (PDIM) (Siegrist M S & Bertozzi C R, 2013). In nature, fatty acids must be activated before they can be assimilated into various metabolic pathways. The universal mechanism of n-fatty acid activation involves conversion of fatty acids by a family of omnipresent fatty acyl-CoA ligases (FACLs). The biosynthesis of PDIM, an alternate mechanism of fatty acid activation, catalyzed by fatty acyl-AMP ligases (FAALs) was established in Mtb (Arora P, 2008).