FilGAP and ArhGAP22 activation by RhoA/ROCK have been suggested to play a role in the RhoA/Rac1 antagonism of tumor cells [27, 28], but inactivation of specific GEFs (p115RhoGEF, LARG, PDZ-RhoGEF) can also contribute to reduced Rac1 activation. The gene discussed is RAC1; the disease is neoplasm.