In a breast cancer model, it was shown how one of the key players in the CSC phenotype formation, β-catenin, is regulated by HSF1 in a phosphorylation-dependent manner: The activating phosphorylation of HSF1 at serine 326 led to HSF1-mediated involvement of the RNA-binding protein HuR (human antigen R), which controls β-catenin mRNA translation [169]. The gene discussed is HSF1; the disease is breast cancer.