The last decade has witnessed a burgeoning of neuroimaging studies substantiating models of atypical brain connectivity in Autism Spectrum Disorder (ASD) – connectopathy. Yet, their promise to lead to clinically useful ASD biomarkers remains unmet. A key challenge has been the variation of neuroimaging findings across studies. In fact, mixed reports of hypo- and/or hyper-connectivity affecting a range of neural circuits have left the precise nature of ASD connectopathy unclear. Additionally, a primary investigative focus on phenomenology has limited the progress on capturing underlying mechanisms. Here, we will introduce state-of the-art multidisciplinary work aimed to address these gaps. To this end, empirical findings from studies on idiopathic and/or genetically determined ASD, using multiscale time and space investigations will be presented. These will be integrated with studies targeting heterogeneity as a source rather than a confound and emphasizing replicability and reproducibility. In doing so, this panel will provide an advanced framework highlighting the next steps necessary for delineating clinically useful biomarkers and discerning the mechanisms at the origin of brain connectopathy in ASD.