Wang, ZL et al. found that acetylcholine increased the self-renewal ability of CD133(+) thyroid cancer cells and promoted the expression of PD-L1 via the CD133-Akt pathway (101).The stimulation of α5nAChR promoted PD-L1 expression and thus induced immune escape via the pSTAT3, Jab1 signaling in lung adenocarcinomas (103).α7nAChRs expressed on antigen-presenting cells downregulated T cell differentiation by inhibiting antigen processing, while those expressed on CD4(+) T cells upregulated differentiation into Tregs and Teffs, regulating the intensity of immune responses (94, 95). The gene discussed is AKT1; the disease is thyroid cancer.