Our present results clearly show that the effectiveness of the combined opposite targeting of p110δ PI3K and RhoA in preventing skin tumour growth is a results of its efficacy to suppress the expression of ATX, which derives from both, the modulation of macrophage recruitment to tumour sites, because of p110δ PI3K inactivation, and the silencing of p190RhoGAP expression in tumour cells. The gene discussed is ARHGAP35; the disease is skin neoplasm.