Further downstream in the cancer care timeline, as we more routinely detect NTRK fusions that make patients eligible for TRK inhibitors, we will also have to consider how our molecular diagnostic tests detect mechanisms of acquired resistance in these patients, both on-target second site mutations in the NTRK kinase domain [49, 50] and alterations that activate bypass signalling pathways [51]. The gene discussed is TPM3; the disease is cancer.