Currently, increasing studies revealed that CYTOR exerted its function as an oncogene at both the cytoplasm and nuclei by disturbing various signaling pathways.[12, 13] To dissect the regulatory mechanism of nuclear expression of CYTOR in TB cells, RNA‐seq was performed in HNSCC cells with depletion of CYTOR, suggesting that FOSL1 has a pivotal role in CYTOR‐mediated HNSCC progression. The gene discussed is FOSL1; the disease is tuberculosis.