Despite extensive sequencing, some GIST remain “wild-type” GIST, but a number have been identified nowadays with the modern techniques to carry low-frequency KIT or PDGFRA mutations, while others were associated with fusions of NTRK (NTRK3-ETV6) and FGFR1 (FGFR1-HOOK3, FGFR1-TACC1), alterations in the RAS-MAPK pathway with BRAF mutations, NF1 mutations, or SDHA deficiency caused by a germline mutation in the suppressor genes encoding the SDH complex or by SDHC promotor methylation [13,14]. This evidence concerns the gene TACC1 and gastrointestinal stromal tumor.