We have shown previously that expression of the GTP-blocked form of the small G protein LdARL-3A/Q70L led to a marked shortening of Leishmania promastigotes flagella. In contrast, there was no effect with the T30N mutant, thought to represent the GDP-blocked form. However, recent data, obtained with human ARF-6, a member of the same family of G proteins, revealed that the corresponding mutant T27N was nucleotide-free and that the GDP-blocked form was the T44N mutant. When expressed in Leishmania, the corresponding new mutant, LdARL-3A/T47N, provoked also flagellum shortening. Then, it is the interruption of the cycling of LdARL-3A between a GDP- and a GTP-bound form which leads to the reduction of the flagellar length. This findings change significantly the understanding and the approaches for studying the mode of action and the role of LdARL-3A.