CTLA4 and melanoma: For example, in HCC, lncRNA Tim3 can stimulate CD8+ T cell exhaustion and promote the survival of these exhausted CD8+ T cells by specifically binding to TIM-3, thereby inhibiting the T cell-mediated antitumor immune response and promoting TIE.184 In melanoma, miR-28 inhibits the expression of TIM-3, PD-1, and CTLA-4, thereby reducing T cell exhaustion and increasing TNF-α and IL-2 secretion, which could enhance the antitumor immune response and inhibit TIE (Table 5).179