It has been previously reported that SOX2‐OT participates in the activation of the AKT‐member of cellular signaling pathways in cholangiocarcinoma [14], as well as being involved in the magnitude of resistance mechanism to EGFR‐TKIs‐based treatment related to the functionality of phosphatase PTEN, reducing AKT phosphorylation in NSCLC [54]. The gene discussed is AKT1; the disease is cholangiocarcinoma.