Although the mechanism by which loss of CYLD function results in perturbation of TRK homeostasis is not fully understood, TRK signaling has been shown to confer a survival advantage to tumor cells by increasing resistance to apoptosis and cell proliferation.4,5,6 This is pertinent because new-generation oral TRK inhibitors are now available, targeting cancers that overexpress TRK after gene rearrangement.7 The gene discussed is NTRK1; the disease is cancer.