The differences between the Cmicro contraction-expansion responses of normal epithelial cells, and mammary carcinoma cells such as T47D (GPER+/ERα+/Erβ+) and SkBr3, to BPA are attributable to high affinity binding of endogenous estradiol (E2) to ERα and GPR30 (Kd, 10−10) [11, 112] delta (Δ)-Cmicro downward shift in Peff with resultant activation of additional anisotropic genes (EGR1 Peff 0.199; CCN2, CTGF Peff 0.166 [22]) [150], inclusive of gene transcription at Δ CmicroPeff 0.184, at which variant ESR1 and FLNA co-express with potential for polymorphism [93, 152]. This evidence concerns the gene EGR1 and breast carcinoma.