reported a multi-institutional analysis of repeat tumour or plasma biopsies from RET+ NSCLC patients treated selpercatinib or pralsetinib, highlighting the role of RET solvent front mutations G810C and G810S as on-target mechanisms of resistance and MET and KRAS amplification as an RET-independent mechanism of escape [62]. Here, KRAS is linked to non-small cell lung carcinoma.