Functionally, ectopic overexpression of either wild type (WT) or constitutively active PKCβI or PKCβII increases breast cancer cell line growth in vitro through upregulation of cyclin D1, while inhibition of kinase activity decreases growth as seen via introduction of dominant negative PKCβI or PKCβII, and through treatment with LY379196, a PKCβ selective inhibitor (22). This evidence concerns the gene PRKCB and breast cancer.