In comparing the pretherapy versus (vs.) the posttherapy samples (n = 32), we observed a significant decrease in ERBB2 and FASN expression, as expected, and a significant increase in CD36 expression (Fig. 1A) in the posttherapy samples, suggesting that trastuzumab-resistant tumor cells could undergo a switch in their FA source from FASN-mediated de novo biosynthesis to FA uptake from the extracellular environment via the reprogramming of CD36 expression/activity [37]. The gene discussed is FASN; the disease is neoplasm.