Take RGS4 protein discussed above as an example: in breast cancer cells, disruption of the interaction between RGS and G proteins will cause the selective inhibition of the GAP-dependent functions of RGS4, while targeting the expression of RGS4, RGS6 and RGS16 can give rise to the effects on both the GAP-dependent and GAP-independent regulations of these RGS proteins. This evidence concerns the gene RGS16 and breast cancer.