The intrinsic resiliency of CSCs in lung cancer is diverse and may be attributed to the following factors: quiescent state with low proliferation rate, [29], activation of drug-efflux processes by the ATP binding cassette (ABC) transporters [30,31], overexpression of DNA-repair mechanisms [18,32], decreased programmed cell death [33], acquisition of an epithelial-to-mesenchymal (EMT) phenotype [34] and ALDH activity [35]. This evidence concerns the gene LDHA and lung carcinoma.