3p-deletion syndrome, characterized by the absence of human chromosome 3p, often reflects Autism Spectrum Disorder (ASD)-like behaviors. Notably, genes of interest, CHL1, CNTN6, and CNTN4, nestled within the genomic locus 3p26.3, are implicated in ASD risk. This study embarks on deciphering the intricate mechanisms orchestrating behavioral and neural shifts. Through transgenic mice lacking these genes (3pKO), we seek to unravel these complexities. To evaluate social ability, anxiety and repetitive behavior, we conducted social interaction test (SIT), Open field test (OFT), and measuring grooming total time. The result in SIT showed that control mice spent about 70% of approaching time for the social partner, but it was about 50% in 3pKO mice, indicating 3pKO mice decreased socialization. The result in OFT showed 3pKO mice spent significantly more time in the central area and the grooming total time was decreased in 3pKO mice, indicating reducing anxiety and repetitive behavior. In addition, histological analysis of brain sections by nissl staining revealed morphological abnormalities in the hippocampus and enlargement of the lateral ventricle in some individuals. We now examine the expression levels of genes related to neurogenesis and autism-related genes in the hippocampus. As we carefully analyze the complex interactions between behavioral, histological, and expression changes in 3pKO mice, a comprehensive understanding unfolds. The significance of CHL1, CNTN6, and CNTN4 genes in shaping hippocampal function and social behaviors urges us to untangle the intricate processes at play, uncovering the underlying scientific mechanism.