**1. Introduction**

Autism spectrum disorder (ASD) represents a group of heterogeneous neurodevelopmental conditions characterized by deficits in social cognition, together with the presence of restricted and/or repetitive patterns of behaviors, activities, or interests [1]. Social cognition refers to those cognitive processes that allow individuals to successfully navigate the challenges of living in a social group. Thus, a functional social cognitive system involves the integration of several domains of behavior including attention, memory, emotion, and motivation to be able to understand identity, potential actions, social hierarchy, and emotional status of a conspecific and therefore guide the appropriate behavioral response [2]. In autism, deficits in social cognition processes are found at multiple levels, such as failure to initiate or respond to social interactions, lack of interest in social situations, abnormal social approach, difficulties expressing and understanding verbal and nonverbal communication (i.e., body language and facial expressions), and problems adjusting behavior to different social situations, among others [1]. Autism affects roughly 1 in 59 children, becoming one of the primary mental health issues

worldwide [3]. In addition to the main symptoms, ASD is usually associated with other behavioral and/or neurological problems, such as hyperactivity, epilepsy, aggression, irritability, sleep problems, gastrointestinal symptoms, and sensory processing abnormalities [4].

Although currently accepted to be highly genetic (over 90% of the risk of developing ASD is due to genetic variation) [5], the etiology of ASD is complex, and its genetic architecture is diverse. Common allelic variation with small effect sizes is responsible for most cases, while rare but highly penetrant mutations that usually lead to other syndromes associated with autism are observed in about 20% of the cases [6]. In addition to genetic factors, exposition to some environmental factors during prenatal periods has also been associated with autism. Some of the most replicated are the intake of valproic acid, a drug used to treat epilepsy, during pregnancy and maternal infections. In all, the combination of interactions between genetic predisposition and environmental factors will determine the development of the disorder [7]. Given the clinical and etiological heterogeneity of ASD, the investigation of its pathophysiology has been challenging. From a research point of view, the study of "single gene" causes of autism, although rare in the population, has been proven to be useful to understand its pathophysiology and develop targeted treatments. In addition, animal models of monogenic causes of autism are easily generated and constitute a critical component of research. Research from both human and animal studies converge in a series of key brain structures and circuits involved in social cognition and their dysfunction in autism. Within these circuits, the cerebellum, traditionally associated with movement control, is becoming an important player in the social brain network. In this chapter, we will first start by describing the social brain circuitry traditionally thought to be affected in autism; we will then present evidence for the role of the cerebellum as a new player in the social circuitry and its role in the pathophysiology of ASD; finally, we will present data from animal models of monogenic causes of ASD in which a cerebellar pathology has been described such as Fragile X syndrome *(FMR1*), tuberous sclerosis syndrome (*TSC1/TSC2)*, and Phelan-McDermid syndrome *(SHANK3*), supporting the role of the cerebellum in social defects. In all, we believe the current evidence grants the need of further research of the cerebellar role in ASD pathophysiology.
