Regardless of the mechanism through which silibinin protects the lipidome of hepatic cells against lorlatinib (e.g., by increasing the shift of fatty acids from triglycerides towards phospholipids and/or increasing the endogenous cholesterol conversion to bile acids), silibinin might represent an idoneous lipid-lowering agent in new treatment regimens for patients with NSCLC at the highest risk of developing brain metastases, such as those continuously exposed to ALK-TKIs [52]. This evidence concerns the gene ALK and non-small cell lung carcinoma.