This adds a new dimension to API’s known antitumor mechanisms—which include reducing oxidative stress via the Nrf2/NF-κB pathway [50,51] or modulating lipid accumulation via XO/NLRP3 [52]—by showing that it also normalizes FAM reprogramming via direct CDK1 binding, supporting its development as a chemopreventive agent for nanomaterial-associated lung cancer. The gene discussed is CDK1; the disease is lung cancer.