Table 3.

Genes and their single nucleotide polymorphisms investigated in association with non-alcoholic fatty liver disease after liver transplantation

Ref.	Etiology/Population	Genes and best 95%CI OR	Key points
	N (no steatosis/steatosis)
Míková et al[37]	Various	Donor TM6SF2: rs58542926 (1.28-4.42); Donor PNPLA3: rs738409 (1.28-3.27); Additive: TM6SF2 + PNPLA3 (2.01-13.0); Recipient NS for all	Donor TM6SF2 A allele and PNPLA3 G allele are associated with steatosis in both univariate and multivariate adjusted analyses
	European
	139/129		The additive effect of donor TM6SF2 A allele and donor PNPLA3 G allele is strongly associated with steatosis
			No association when recipients SNPs were analyzed
John et al[40]	HCV	Recipient adiponectin: rs1501299 (1.09-5.5), rs266729 (0.14-0.75); rs2241766, rs17300539 – NS; Donor – NS for all	Recipient but not donor adiponectin rs1501299 GG genotype is significantly, but weakly associated with de novo steatosis after adjustment for race and HCV genotype
	North American
	72/39
Kim et al[39]	Various	Recipient PNPLA3: rs738409 (1.00-9.34)1; Donor – NS; Additive donor + recipent: (1.32-117.0)2	If both, donor and recipient have G allele, the recipient has higher risk for steatosis weak association, small number of patients
	Eastern Asian
	23/9
Trunečka et al[38]	Various	Donor PNPLA3: rs738409 (1.05-1.75); Recipient PNPLA3: rs738409 (1.02-1.57)	PNPLA3 G allele in donors [OR (95%CI) = 1.62 (1.12-2.33)], but not in recipients is independently associated with steatosis after adjustment for age, disease etiology, BMI, diabetes, hypertension, therapy and lipids
	European
	89/87

¹Calculated from study data for log-additive model by authors of this review.

²Calculated from study data by authors of this review. BMI: Body mass index; HCV: Hepatitis C virus; N-number; NS: Not significant; OR: Odds ratio; PNPLA3: Patatin-like phospholipase domain-containing 3; SNP: Single nucleotide polymorphism; TM6SF2: Transmembrane 6 superfamily member 2; 95%CI OR: 95% confidence interval for odds ratio.