In addition, we noticed that the addition of the CaM antagonist W-7 to breast adenocarcinoma SK-BR-3 cells induced the concomitant inhibition of ErbB2 and the Akt and ERK1/2 (extracellular-regulated kinases 1 and 2) pathways as expected, while the phosphorylation (activation) of CREB (cAMP response element-binding protein) and ATF1 (activating transcription factor-1) increased, most likely due to the absence of the CaM/calcineurin-mediated dephosphorylation of these transcription factors [66]. The gene discussed is ERBB2; the disease is breast adenocarcinoma.