In particular, the reprogramming of CD36-mediated FA uptake in lipogenic HER2 + BC constitutes a mechanism of resistance to HER2-targeted drugs by fulfilling the requirement for lipids that is compromised by pharmacological inhibition of the HER2-FASN axis following treatment with HER2 and/or FASN inhibitors, as recently observed in preclinical and clinical colorectal cancer models [50]. The gene discussed is CD36; the disease is colorectal cancer.