The inverse correlation of de novo FA and phospholipid metabolites with the expression level of HMGCS1, HMGCS2, HMGCR, BDH1, and OXCT1 (Fig. S4-2a, 3b, 9b, and 10a in the “Electronic Supplementary Material”) suggests that orlistat treatment in NSCLC cells activates alternative metabolic pathways for energy production such as ketone and cholesterol synthesis as a compensatory response to FASN inhibition. This evidence concerns the gene HMGCS1 and non-small cell lung carcinoma.