Saji et al. crossed Akt1 knockout mice with TRβ knockin mice; the resulting TRβ-PV/PV-Akt1 knockout mice exhibited delayed development of thyroid cancer with a less invasive phenotype, which indicated that the development and progression of thyroid cancer were Akt1-dependent in this mouse model [147]. This evidence concerns the gene THRB and thyroid gland carcinoma.