While animal studies will further validate antitumorigenic efficacy, the suppression of tumor initiation (Figures 2 and 3) and self-renewal of CSCs (Figures 4 and 5) in various human lung cancer cells, namely, H460 (p53 and KRas wild type), H23 (p53 and KRas mutant), and A549 (KRas mutant), markedly observed after treatment with TDB (5–10 μM) strongly support the CSC-targeted potential of this bibenzyl compound. Here, KRAS is linked to lung cancer.