**2. Targets and action mode of active principles currently used in the treatment of TB**

Current TB chemotherapy is based on the combination of four anti-TB drugs which inhibit the bacterial metabolism, particularly the cell wall synthesis [5]. During the therapy, the goal of this drug combination strategy is to prevent effectively the mutational events [6]. According to their actionmode,firstandsecondlineanti-TBdrugsaregroupedintocellwallinhibitors (INH,EMB, ethionamide (ETH), and cycloserine (DCS)), protein synthesis inhibitors (RIF, fluoroquino‐ lones, STR, kanamycin (KAN)), and membrane energy metabolism inhibitors (PZA).

Current chemotherapy principally inhibits cell processes such as cell wall biosynthesis and DNA replication, and they only turn to be active regarding bacteria in active growth [5]. This implies that the chemotherapeutic agents in use are efficient bactericides but are poor steri‐ lizers, not able to kill "dormant" *M. tuberculosis* which persists in macrophages after the death of the active bacteria [5]. RIF and PZAhave a partial sterilizing activity and they play an important role in the decrease of therapy from 18 to 6 months, even though there is a persistent population surviving these two agents. Consequently the current therapy ensures a clinical cure but fails to obtain a bacteriological cure [5].
