For example, the hypoxic conditions seem to reverse the pro-tumoral phenotype of the CAFs, observed with the impairment of the ECM remodeling and CAF-induced cell invasion, through a mechanism dependent on the inhibition of PHD2 through low oxygen levels and the consequent stabilization of HIF-1α in a breast cancer model, making PHD2 in CAFs a probable therapeutic target [172,173]. The gene discussed is EGLN1; the disease is breast cancer.