As shown in Fig. 5b, the kinase activity assay demonstrated that silencing of IGFBP7 in various thyroid cancer cells markedly promoted, whereas overexpression of IGFBP7 suppressed, endogenous AKT activity, as demonstrated by the phosphorylation levels of a common AKT substrate, GSK3β. The gene discussed is IGFBP7; the disease is thyroid gland carcinoma.