To further understand the role of TIM-3 in HNSCC development and progression, Liu and colleagues observed that the in vivo inhibition of TIM-3 in a preclinical immunocompetent mouse model controlled tumor growth by restoring the immune response, particularly increases the frequency of Teff in tumor and LN through modulation of TIM-3 expression in these cells and reduces the recruitment of MDSCs into the TME in a CXCL1 dependent-manner [84]. The gene discussed is CXCL1; the disease is neoplasm.