Leptynia specimens were analyzed by karyotype analysis, mitochondrial gene sequencing and SEM of bodies and eggs. Here we describe a new species, Leptynia annaepaulae, and three subspecies of L. attenuata Pantel (L. attenuata attenuata, L. attenuata iberica, L. attenuata algarvica). The phylogeny of the genus Leptynia is congruent with a karyotype trend toward a reduction of chromosome number and the shift from the shared XX/X0 sex chromosome formula to the unusual XX/XY one. Chromosome repatterning appears to occur ahead of genetic differentiation, following a chromosome model of cladogenesis. Chromosome and genetic differentiation, in turn, appears to precede morphological distinction, thus realizing a condition of incipient species for most of the Leptynia taxa. Actually, morphological analyses revealed that, only rarely clear cut differences exist among and between taxa, while, more often, just trends in the differentiating traits occur, since the investigated characters generally suffer from some overlapping: In this study, only the 10th:9th ratio value and the subanal vomer appear to be diagnostic for L. annaepaulae against all other Leptynia taxa. As a consequence, the subanal vomer as well as cercus tooth features with egg chorion traits are not sharply diagnostic for the remaining co-generic taxa; however, comparisons are quite helpful in reducing uncertainties. A likely phylogeographic scenario for the genus supports that Leptynia ancestors spread from Northern Africa into Southern Spain where an ancestral taxon originated L. annaepaulae (2n = 40/39, XX/X0, with 2 large dibrachial pairs). Later on, a northbound colonization, should have originated L. caprai (2n = 40/39, XX/X0, all acrocentrics), from which L. montana (2n = 38, XX/X0) and L. attenuata (2n = 36, XY/XX) originated; supporting instances of chromosome repatterning have been actually observed. In this connection we like to stress that, particularly in stick insects, androgenesis has been a preferential pathway to quickly make homozygous those odd chromosome rearrangements likely responsible for low fitness in the heterozygotes.