Given the improvements in prognosis and survival of patients with ALK translocations, a better understanding of the primary causes underlying lorlatinib-triggered hypercholesterolemia/hypertriglyceridemia might inform new therapeutic strategies to prevent or manage the undesirable lipid-modifying activity of lorlatinib in patients with ALK-positive NSCLC. This evidence concerns the gene ALK and non-small cell lung carcinoma.