The findings substantiate the oncogenic roles of CD24 in OSCC, which are consistent with its upregulation in tumors and the poor prognosis of patients.22, 23, 24, 25 Although the discrepancy in the final tumor burden of control tumors and Doxy-induced tumors in MOC-L1 is not so eminent, which might be due to the growth of control tumors in the plateau phase or the shortage of Doxy induction, targeting of CD24 using inhibitors or monoclonal antibodies could be a promising strategy for OSCC interception.25 The gene discussed is CD24; the disease is neoplasm.