Further studies using molecular docking and animal models confirmed the B4’s therapeutic potential against pneumonia induced by Klebsiella pneumoniae or influenza virus FM1 through modulation of the TLR4/Myd88 signaling pathway.[3] Tianling Lou et al validated the predictions from network pharmacological results using a mouse model of pneumonia induced by Pseudomonas aeruginosa. This evidence concerns the gene MYD88 and susceptibility to pneumonia measurement.