To test the hypothesis that RAC1 gene copy increases could be potentially targetable in principle, we determined the sensitivity of several newly developed in-house HNSCC patient-derived tumor cultures (PDCs) that harbored different RAC1 gene copy numbers, including RAC1-diploidy PDCs (QM47-PDC & QM43-PDC: CN = 2) and RAC1-gain (T11-PDC: CN = 3) and RAC1-amp (T76-PDC: CN = 4), towards a recently developed preclinical Rac inhibitor, EHop-016, in 3D culture conditions [37]. The gene discussed is AKT1; the disease is neoplasm.