Autism spectrum disorder (ASD) is a complex and highly prevalent neurodevelopmental disorder. ASD exhibits significant heterogeneity in genotypes and phenotypes. In recent years, dysregulation of protein synthesis has emerged as a converging mechanism in ASD. Here, to explore altered translation in ASD, we used induced pluripotent stem cells (iPSCs) which have emerged as a promising cellular tool for disease modeling. Patient relevant mutations in FMR1, PTEN, and TSC2, that cause dysregulated protein synthesis, were introduced into iPSCs derived from healthy donors via CRISPR/Cas9. Then, iPSCs were differentiated into both iNeurons and cortical organoids to study their proteome using mass spectrometry (MS). After analysing the results, we can see that TSC2 and PTEN mutants present a similar profile in both models (iNeurons and organoids), but not for FMR1. GO enrichment analysis of proteins showed an increase in the abundance of proteins associated with mitochondrial processes, such as cellular respiration, protein synthesis and structural proteins. These results are in line with the literature and reflect the hyperactivation of mTORC1 related to the PTEN and TSC2 mutations, which require a higher energy production in the cell. Downregulated proteins instead are related to transcriptional and epigenetic regulation. Interestingly, we observed significant enrichment of genes that have been previously linked to ASD (SFARI gene list) among dysregulated proteins, highlighting the functional relevance of the proteomic data. Consequently, the results of this research are expected to elucidate the molecular underpinnings of ASD, encompassing not only case-specific mutations, but also alterations shared between different ASD-related mutations.