Even though a possible delay in the duplication time of intracellular amastigotes caused by the presence of Olaparib or an effect of this compound on the amastigotes-to-trypomastigote differentiation cannot be discarded, the results here obtained, taken together with data published by other authors, suggest a possible interference of Olaparib with the generation of the most adequate conditions needed for the persistence of the infection, in which PARP-1 from the host cell would be intimately involved. The gene discussed is PARP1; the disease is infection.