The function of the protein derived from CTNNA1-ALK fusion was previously unknown, since only one study described CTNNA1 as a fusion partner of ALK in a patient with salivary secretory carcinoma, and the treatment outcomes were not reported.26 Our case of CTNNA-ALK–positive parotid adenocarcinoma demonstrated rearrangement in the canonical exon 20 recombination region and showed a clinical response to alectinib (Appendix Fig A1B and Table 2); this was consistent with the other cancer types in our series that had an ALK fusion in the same region and also demonstrated a response to alectinib. This evidence concerns the gene ALK and cancer.