ER-positive resistance in breast cancer is also attributed to the activation of growthfactor pathways, such as HER2, IGF-1R and FGFR and stress-related kinases, such as AKT,JNK, MAPKs, c-SRC and others, that regulate posttranslational modifications of the ER andits coactivators that increase the receptor activity (Schiff et al. 2004, Shouet al. 2004, Santenet al. 2009b, Theoret et al. 2011). This evidence concerns the gene ERBB2 and breast carcinoma.