For example, Solomon et al. demonstrated using cfDNA samples from a patient with CCDC6–RET NSCLC with prior dramatic response to selpercatinib the emergence of RET G810C mutation at the time of progression.59,60 In addition to G810 mutations, other RET-independent resistance mechanisms have also been reported in RET inhibitor-treated patients including amplifications of MET and KRAS genes.61,62NTRK3 fusion as a mechanism of resistance has also been reported in RET fusion-positive lung cancer.63 This evidence concerns the gene KRAS and non-small cell lung carcinoma.