Table 1. Commonly observed ASD-related DEGs in this and previous studies.

Genes suggested by previous human studies						Description
Voineagu et al. (2011)	Pinto et al. (2014)	Sanders et al. (2015)	Bourgeron et al. (2015)a)		Chang et al. (2015)
					actn4	alpha-actinin-4
adsl						adenylosuccinate lyase
		capn12				calcium-activate neutral proteinase 12
	dcx (dcxr)					dicarbonyl/L-xylulose reductase
					ddb1	damage-specific DNA binding protein 1
					eif4a1 (eif4a1a)	eukaryotic translation initiation factor 4A1A
					fanca	fanconi anaemia group A protein
	gamt					guanidinoacetate N-methyltransferase
	gatm					glycine amidinotransferase (L-arginine:glycine amidinotransferase)
	hsd17b10					hydroxysteroid (17-beta) dehydrogenase 10
	kcnj11					potassium inwardly rectifying channel, subfamily J, member 11
	mbd5					methyl-CpG binding domain protein 5
					myh11 (myh11a)	myosin, heavy chain 11a, smooth muscle
			nrxn2			neurexin-2
pde9a						high affinity cGMP-specific 3',5'-cyclic phosphodiesterase 9A
					pfkm	6-phosphofructokinase, muscle type
	rpe65 (rpe65a)					retinal pigment epithelium-specific protein 65a
rpl10						ribosomal protein L10
shank3 (shank3a)						SH3 and multiple ankyrin repeat domains 3a
		slc6a1				solute carrier family 6, member 1, like
suclg2						succinate-CoA ligase, GDP-forming, beta subunit
tdo2						tryptophan 2,3-dioxygenase a
		trip12				thyroid hormone receptor interactor 12
tsc1(tsc1b)			tsc1 (tsc1b)			tuberous sclerosis 1b

^a) Review article. DEGs were determined based on statistical significance (p < 0.05). Fold changes (log₂FC) for each DEG are shown in S3–S7 Tables. DEGs from multiple studies are marked in bold.