Based on the working hypothesis of P-gp-dependent collateral sensitivity [14–17], we examined the ability of tamoxifen as a collateral sensitivity drug for two reasons: a) tamoxifen has been previously shown to activate P-gp ATPase at clinically achievable concentration (4–6 μM) [20, 21], and b) tamoxifen is widely used in the treatment of estrogen receptor-positive breast cancer [22]. This evidence concerns the gene PGP and breast cancer.