In conclusion, in addition to previous findings which identified the Kv11.1 K+-uptake channels of the CMs as targets of CFZ and BDQ, the results of the current study have also identified the Na+,K+-ATPase of the CMs as a potential target of these antibiotics, suggesting inhibitory effects of the antibiotics on the Na+,K+-ATPase as possible contributors to the development of QT prolongation in TB patients. This evidence concerns the gene KCNH2 and tuberculosis.