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ASD signs and symptoms appear early in development before the age of 3\u00a0years. It is unlikely for a person to acquire autism after a period of normal development. However, we encountered an 8-year-old child who developed ASD later in life although his developmental milestones were normal at the beginning of life. Sequencing the complete coding part of the genome identified a hemizygous nonsense mutation (NM_001367857.2):c.1803C&gt;G; (p.Tyr601Ter) in the gene (<jats:italic>SATL1<\/jats:italic>) encoding spermidine\/spermine N1-acetyl transferase like 1. Screening an ASD cohort of 28 isolated patients for the <jats:italic>SATL1<\/jats:italic> gene identified another patient with the same variant. Although <jats:italic>SATL1<\/jats:italic> mutations have not been associated with any human diseases, our data suggests that a mutation in <jats:italic>SATL1<\/jats:italic> is the underlying cause of ASD in our cases. In mammals, mutations in spermine synthase (<jats:italic>SMS<\/jats:italic>), an enzyme needed for the synthesis of spermidine polyamine, have been reported in a syndromic form of the X-linked mental retardation. Moreover, <jats:italic>SATL1<\/jats:italic> gene expression studies showed a relatively higher expression of <jats:italic>SATL1<\/jats:italic> transcripts in ASD related parts of the brain including the cerebellum, amygdala and frontal cortex. Additionally, spermidine has been characterized in the context of learning and memory and supplementations with spermidine increase neuroprotective effects and decrease age-induced memory impairment. Furthermore, spermidine biosynthesis is required for spontaneous axonal regeneration and prevents \u03b1-synuclein neurotoxicity in invertebrate models. 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