Although specific molecular mechanisms detailing the interaction between biochanin-A and NLRP3 are not well established in IPF, the compound’s cardiac and neuroprotective effects have been associated with triggering the PI3K/Akt cascade and preventing the MAPK signaling cascade, indicating potential molecular crosstalk that could regulate the NLRP3 inflammasome. The gene discussed is NLRP3; the disease is idiopathic pulmonary fibrosis.