Autism spectrum disorders (ASD) are associated with a high genetic heterogeneity, yet for many of the cases, the underlying molecular causes remain elusive. While several studies have elucidated some distinct patterns, fundamental questions persist: How do mutations dispersed across numerous genes lead to the development of a phenotypically similar disorder? Essentially, it remains largely unclear whether mutations in distinct genes lead to similar molecular and cellular states within the brain. Thus, it is important to identify molecular mechanisms responsible aiming to decipher points of convergence and divergence.By making use of single-nucleus multi-omic technologies, which enable simultaneous snRNA-seq coupled with snATAC-seq, we profiled ~200.000 cells obtained from 251 samples collected from 11 ASD mouse lines throughout neurodevelopment. To study potential sex effects, we analyzed all time points and genotypes in both females and males. With this dataset, we were able to explore points of convergence and divergence, affected time windows, and disparities between sexes.We found that mutations in the selected genes primarily influence the molecular profile of the cerebral cortex during a specific time frame. Additionally, we could delineate both the nature of molecular convergence across mutants and their distinctions. Interestingly, when focusing on differences between males and females, significant differences are captured, providing insight into the sex-specific intricacies of ASD at a molecular level.