Moreover, the levels of Ser33-phosphorylated β-catenin which lead to the proteasomal degradation of β-catenin were significantly increased in BC cells treated with HISLA-silenced TAMs-exo, while the expression of GSK3β which is responsible for Ser33-phosphorylation of β-catenin was not affected during si-HISLA or si-Control TAM-exo-treated BC cells (Figures 5(a) and 5(b)). The gene discussed is GSK3B; the disease is breast cancer.