For both low-grade and high-grade tumours, opportunities for repurposing currently FDA-approved targeted therapies are limited given infrequent mutation in the common driver genes such as BRAF, EGFR, HER2 and KIT. KRAS, once thought to be undruggable, has now been effectively targeted with covalent binders specifically to the cysteine in the G12C mutation. The gene discussed is BRAF; the disease is neoplasm.