EGFR and triple-negative breast carcinoma: Sustained activation of ERK1/2 by overexpression of constitutively active MEK1 was sufficient to expand CD44+/CD24− cell populations in which EGFR activity was blocked by either Erlotinib, an EGFR kinase inhibitor, or BB-94, a metalloprotease inhibitor, suggested that metalloprotease-dependent activation of EGFR modulated CD44+/CD24− in triple-negative breast cancer cells through the MEK/ERK pathway [123].