As demonstrated by Liu et al., after transfection with exogenous B7-H3, several breast cancer cell lines with B7-H3 overexpression dramatically enriched their CSC population, which was marked by CD24 and CD44, while B7-H3 knockdown led to the opposite results, and these effects were mediated via the B7-H3/MVP/MEK pathway [58]. This evidence concerns the gene CD276 and breast carcinoma.