Blocking this function would improve T cell persistence at the tumor site; (ii) the expression of FasL by some stromal cells has been shown to trigger TILs apoptosis therefore participating to the immunotherapy resistance [101,102,103]; (iii) Fas expressed on memory T cells induces the precocious differentiation of naïve Fas-expressing T cells that limits their anti-tumor action through an Akt-dependent pathway [122]. The gene discussed is AKT1; the disease is neoplasm.