In line with the prediction that disrupting the RAC1–p110β interaction might phenocopy deletion or inactivating mutation of Prex2, melanomas arising in the BRAF PTEN PIK3CBmut model were acutely sensitive to MAPK inhibition in the short term, and mice exhibited prolonged overall survival and a delay in the onset of therapeutic resistance compared with BRAF PTEN controls (Fig. 4C; Supplementary Fig. S8E). The gene discussed is PREX2; the disease is melanoma.