The role of the EGFR family in the emergence of PTX resistance was suggested in a series of studies: (i) gefitinib and lapatinib reversed PTX resistance in prostate, breast, and ovarian cancer cells via the direct inhibition of P-gp and drug efflux [45–47]; (ii) the expression of constitutively active EGFR and HER2 induces PTX resistance via increases in class IVa and IVb β-tubulin [48]; (iii) the overexpression of ErbB2 inhibits PTX-induced apoptosis via p21-dependent mechanisms [49, 50]; and (iv) ErbB3 contributes to PTX resistance via PI3K/Akt-mediated up-regulation of survivin [51]. This evidence concerns the gene AKT1 and ovarian cancer.