The vast majority (95.8%) of anaplastic thyroid cancers had genetic alterations resulting in activation of both the PI3K and MAPK pathways, including frequent co-existence of receptor tyrosine kinase copy number gain and gene mutation, as well as PIK3CA, PIK3CB, and PDK1 copy number gains, PTEN mutation and BRAF mutation. Here, PIK3CB is linked to thyroid gland undifferentiated (anaplastic) carcinoma.