Very different cellular models, such as human lymphoma cells or primary cerebellar granule neurons, suggest the inhibition of caspase-induced apoptosis by RAC1, whereby AKT-dependent pro-survival pathways and the consequent Bcl-2-associated death protein (BAD) phosphorylation were downstream and activated by RAC1 [59, 61]. The gene discussed is RAC1; the disease is lymphoma.