Among them, it was demonstrated that cellular stress, such as oxidative stress or hypoxia, in primary TNBCs or ERα-negative BC cell lines, increases the phosphorylation of GR on S134, thus potentiating stress signaling mediated by GR activation leading to an increase in the expression of breast tumor kinase BRK, known as protein tyrosine kinase 6 (PTK6), essential for aggressive BC phenotypes [115]. The gene discussed is PTK6; the disease is breast cancer.