While our study was not designed to investigate the precise molecular mechanisms involved in the hepatic alterations in cholesterol and triglycerides homeostasis in response to lorlatinib, it is reasonable to suggest that there is overlap in the targeted pathways for ALK-rearranged NSCLC growth and those that regulate hepatic function, leading to on-target or closely related off-target hepatic toxicity. The gene discussed is ALK; the disease is non-small cell lung carcinoma.