Nonetheless, because activation of HER2 signaling pathways and proliferation genes in ER+ luminal B-like breast cancer can occur independently of HER2 overexpression via overproduction of HER ligands [54,56], it is not surprising that FASN has also been found to operate as a key enabler of tamoxifen resistance in luminal B-like ER+/HER2- breast cancer cells, exhibiting a persistent promotion of HER2/HER3 signaling due to the overexpression of the HER3 ligand heregulin [57]. The gene discussed is ERBB2; the disease is breast cancer.