Notably, knocking down the αv subunit resulted in a more pronounced reduction in CD47 surface expression than knocking down the β3 subunit, suggesting the involvement of other integrins that interact with αv to form heterodimers (Figure S6A, Supporting Information) and contribute to CD47 stabilization in cancer cells.[19] To explore this further, we examined the gene expression of several integrins (ITGA2B, ITGA5, ITGB1, ITGB6, and ITGB8) in MDA‐MB‐231 cells, revealing relatively high expression levels of ITGA5, ITGB1, and ITGB6 (Figure S6B, Supporting Information). The gene discussed is ITGB8; the disease is cancer.