Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive therapy for neuropsychiatric conditions, yet its cellular mechanisms are not well understood, limiting its optimization. Our lab uses transgenic mice lacking ephrin-A2 to study the effect of low-intensity (LI) rTMS on neural circuitry. Ephrin-A2-/- mice have abnormal supernumerary projections in the retinocollicular pathway, and we previously showed that chronic LI-rTMS removes ectopic terminations in the superior colliculus (SC) in these mice. However, anterograde tracing cannot determine if ectopic projections in the transgenic mice stem from incorrectly projecting retinal ganglion cells (RGCs) or aberrant branching, limiting our understanding of LI-rTMS mechanisms. To address this, we employed dual-colour retrograde tracing from the SC to test whether (1) ectopic projections are due to abnormal branching (double-labelled RGCs) and (2) if LI-rTMS reduces these ectopic branches. Adult ephrin-A2-/- mice were assigned to LI-rTMS or control groups, receiving 10 daily sessions of LI-rTMS or no treatment. Post-stimulation, animals underwent stereotaxic injection of Hoechst 33342 and DiI into the rostral and caudal SC to retrogradely label RGCs. Retina wholemounts were analysed 1 week after the injections. All control animals (n=4) had double-labelled RGCs (0.84% ± 0.68 of total labelled RGCs), indicating ectopic projections arise from abnormal branching. Preliminary data from an LI-rTMS-treated mouse suggest LI-rTMS does not reduce double-labelled RGCs (0.33% double-labelled RGCs) compared to controls. Our results contradict previous findings, suggesting ectopic projections in ephrin-A2-/- mice may originates from both aberrant branches and incorrectly projecting RGCs, with LI-rTMS affecting only the latter.