As thyroid cancers tend to be more resistant to traditional therapies that target specific oncogenic drivers, such as the BRAF inhibitor vemurafenib [18], we hypothesized that we may be able to uncover additional metabolic therapeutic targets that, when inhibited, may act as circuit breakers to prevent the reprogramming associated with resistance to many tyrosine kinase inhibitors. The gene discussed is BRAF; the disease is thyroid cancer.