As described earlier, the overabundance of T-type Ca2+ channels in ovarian cancer leads to PI3K/AKT overexpression and, consequently, treatment with mibefradil, which is a calcium channel blocking agent, decreased nuclear FOXM1 protein levels and its binding to the BIRC5 (survivin) promoter in EOC cells [153]. The gene discussed is AKT1; the disease is ovarian carcinoma.