Autism is an extremely heterogeneous neurodevelopmental disorder characterized by delays in social interaction and communication skills, stereotypical behavior, narrowed interests and limited activities. Its prevalence is about 1% of the world population. Its prevalence is increasing, and it is approximately four times more common in boys than girls. Comorbid conditions such as cognitive impairment, epilepsy, psychiatric diseases, nutritional disorders, gastrointestinal diseases and abnormal dysbiotic conditions, sleep disorders, and dysmorphism are frequently encountered in individuals with autism. Although the etiopathogenesis of autism is still unclear, the most accepted causality hypothesis is the interaction of multiple factors. Among the underlying causes of autism; genetic predisposition, epigenetic, neurological factors, metabolic factors, psychosocial factors, prenatal/postnatal factors, mitochondrial dysfunction, cellular stress, environmental and immunological-inflammatory factors and the interactions of these factors with each other are shown. These are thought to lead to neurotransmitter imbalance, dysfunctional neuronal pathways, abnormal synaptogenesis and neuronal connectivity. The aim of this review is to address the etiology of autism in the light of current information and to draw attention to the fact that defects in different biological mechanisms lead to autism by reaching a similar result.