Sequence analysis suggested that the extracellular two leucine‐rich repeat (LRR) domains of SLITRKs, and a conserved region in the intracellular carboxyl terminus have a high degree of consensus with the last 16 amino acids of NTRK, encoded tropomyosin‐related kinase (TRK).[6] NTRK aberrations, such as overexpression or gene fusion, have been implicated in the pathogenesis of many cancer types.[27] The activation of NTRK leads to several downstream signaling pathways, including PI3K/Akt, MEK/ERK, and NFκB.[28, 29] Therefore, SLITRK4 overexpression showed similarity with the NTRK‐like pathway. The gene discussed is AKT1; the disease is cancer.