It has been reported that in the immune microenvironment of lung cancer, the interaction of co-stimulatory molecules CD40 and CD154 (CD40L) molecules on the surface of B cells resulted in an enhanced ability of activated B lymphocytes to present antigens to CTL cells, leading to a significant increase in the levels of IFN-γ and IL-2 secreted by CTL cells and enhanced the killing effect of CTL on lung cancer stem cells [13]. The gene discussed is IL2; the disease is lung carcinoma.