Yang et al. (2021) showed that Sal-B attenuates NSCLC metastasis through metabolic reprogramming independent of PKM2, revealing its therapeutic promise in the treatment of NSCLC. Han et al. concluded that Sal-B inhibited TGF-β1 and thus induced EMT and migration in A549 cells, hindered cell cycle progression, and promoted cell autophagy and apoptosis. In addition, Sal-B altered the phosphorylation of the MAPK signaling pathway and Smad2/3, especially Smad3 in the junctional region, leading to a decrease in the protein expression of PAI-1 in TGF-β1-stimulated A549 cells (Han et al., 2022). This evidence concerns the gene SMAD2 and non-small cell lung carcinoma.