Under tumor development, TILs face a hostile environment that induces exhaustion to impair their antitumor activity (Boldajipour et al., 2016; Beckermann et al., 2017), which is characterized by the up-regulation of immune checkpoints, such as CTLA-4, PD-1, and Tim-3 (Ahmadzadeh et al., 2009). This evidence concerns the gene HAVCR2 and neoplasm.