Medullary Thyroid Cancer is an intrinsically different disease to its DTC counterpart and requires a nuanced personalised approach to management. Early spread to local lymph nodes is a classic presentation in MTC with nodal disease evident in up to 50% of patients at diagnosis. Surgery remains as the mainstay of treatment for the majority of MTC. Calcitonin and CEA doubling time can assist in prognosticating but there have been advances in both histological and imaging staging. A novel histological grading system has recently been developed involving three histological features which divide into low, intermediate, and high grade which correlates with prognosis. Imaging modalities improving detection and characterisation of metastatic disease have also been developed with various radiolabelled somatostatin analogue including 68Ga-DOTATATE and 68Ga-DOTATOC together with 18F-DOPA, 18F-FDG reviewed for MTC patients. Persistent and metastatic disease treatments have evolved with targeted kinase therapy especially for those harboring RET germline or somatic variants. Successful phase III trials for multikinase inhibitors (vandetinib and cabozantinib) improved progression free survival but rendered patients with significant adverse effects limiting treatment efficacy. Recently, novel more selective RET kinase inhibitors (selpercatinib and pralsetinib) have by contrast been far better tolerated and have impressive PFS improvements. Phase III trials are ongoing with selperatinib and pralsetinib vs physicians choice cabozantinib or vandetinib aiming to delineate the best sequence of treatment. Selection pressures from TKIs can lead to secondary somatic mutations and prevailing of specific genetic clones and ultimately clinical progression. In addition acquired, “on-target” resistance to selective RET inhibition have led to solvent front mutations rendering the selective kinase inhibitors less effective. These mechanisms of resistance are one of the new challenges these successfully treated cohorts are facing and novel strategies including analysis of circulating tumour DNA (ctDNA) from liquid biopisies may assist in identifying these resistant clones earlier.