Furthermore, the results in the co-culture model showed that IL-17 A stimulation reversed the promotional effects of CARHSP1 knockdown on T cell-mediated cancer cell killing, indicating that CARHSP1 partially depended on IL-17 A/IL-17RA to participate in the suppression of the anti-tumor immune microenvironment (Fig. 7G). The gene discussed is CARHSP1; the disease is cancer.