Nonetheless, optimal guidance for the use of newer treatment regimens is urgently needed, as alarming recent reports have suggested the emergence of acquired resistance to newer anti-TB drugs (such as delamanid, with mutations in the fbiA and fgd1 genes) due to inadequate MDR-TB and extensively drug-resistant TB (XDR-TB) treatment regimens for individuals who already have infections resistant to quinolone and other second-line anti-TB drugs [31, 32]. Here, FGD1 is linked to infection.