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Correction

Correction: A missense variant in Mitochondrial Amidoxime Reducing Component 1 gene and protection against liver disease

  • Connor A. Emdin,
  • Mary E. Haas,
  • Amit V. Khera,
  • Krishna Aragam,
  • Mark Chaffin,
  • Derek Klarin,
  • George Hindy,
  • Lan Jiang,
  • Wei-Qi Wei,
  • Qiping Feng,
  • Juha Karjalainen,
  • Aki Havulinna,
  • Tuomo Kiiskinen,
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In this article, the genetic variant PNPLA3 p.I148M is misreported in several sentences as PNPLA3 p.I48M. The variant TM6SF2 p.E167K is misreported in one sentence as TM6SF2 p.E40K.

In the Introduction, the third sentence of the second paragraph:

For example, PNPLA3 p.I48M and TM6SF2 p.E40K, although initially identified as associated with hepatic steatosis [9,10], strongly predispose to the development of alcoholic cirrhosis [11], non-alcoholic cirrhosis [12,13] and hepatitis C-related cirrhosis [14,15].

should read:

For example, PNPLA3 p.I1148M and TM6SF2 p.E167K, although initially identified as associated with hepatic steatosis [9,10], strongly predispose to the development of alcoholic cirrhosis [11], non-alcoholic cirrhosis [12,13] and hepatitis C-related cirrhosis [14,15].

In the Results, the fourth sentence of the first paragraph:

We examined the association of all-cause cirrhosis with six genetic variants previously reported to be associated with alcoholic or non-alcoholic cirrhosis: PNPLA3 I48M, TM6SF2 E167K, MBOAT7 rs641738, HSD17B13 rs72613567, HFE C282Y and SERPINA1 E366K [11,16,18,19].

should read:

We examined the association of all-cause cirrhosis with six genetic variants previously reported to be associated with alcoholic or non-alcoholic cirrhosis: PNPLA3 I148M, TM6SF2 E167K, MBOAT7 rs641738, HSD17B13 rs72613567, HFE C282Y and SERPINA1 E366K [11,16,18,19].

In the Methods, the first sentence of the first paragraph:

To examine whether known alcoholic and non-alcoholic cirrhosis variants associate with all-cause cirrhosis, we tested the association of six known cirrhosis variants (PNPLA3 I48M, TM6SF2 E167K, MBOAT7 rs641738, HSD17B13 rs72613567, HFE C282Y and SERPINA1 E366K [11,16,18,19]) with all-cause cirrhosis in UK Biobank (hospitalization or death due to ICD codes K70.2, K70.3, K70.4, K74.0, K74.1, K74.2, K74.6, K76.6, or I85).

should read:

To examine whether known alcoholic and non-alcoholic cirrhosis variants associate with all-cause cirrhosis, we tested the association of six known cirrhosis variants (PNPLA3 I148M, TM6SF2 E167K, MBOAT7 rs641738, HSD17B13 rs72613567, HFE C282Y and SERPINA1 E366K [11,16,18,19]) with all-cause cirrhosis in UK Biobank (hospitalization or death due to ICD codes K70.2, K70.3, K70.4, K74.0, K74.1, K74.2, K74.6, K76.6, or I85).

There is an error in Table 1. The name p.I48M appears instead of p.I148M.

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Table 1. DNA sequence variants associated with all-cause cirrhosis in the discovery analysis.

https://doi.org/10.1371/journal.pgen.1009503.t001

There is an error in the label of S1 Fig. The name p.I48M appears instead of p.I148M. The authors have provided a corrected version here.

Supporting information

S1 Fig. Risk of alcoholic, non-alcoholic and hepatitis C cirrhosis associated with PNPLA3 I148M, TM6SF2 E167K and HSD17B13.

https://doi.org/10.1371/journal.pgen.1009503.s001

(PDF)

Reference

  1. 1. Emdin CA, Haas ME, Khera AV, Aragam K, Chaffin M, Klarin D, et al. (2020) A missense variant in Mitochondrial Amidoxime Reducing Component 1 gene and protection against liver disease. PLoS Genet 16(4): e1008629. https://doi.org/10.1371/journal.pgen.1008629 pmid:32282858

Citation: Emdin CA, Haas ME, Khera AV, Aragam K, Chaffin M, Klarin D, et al. (2021) Correction: A missense variant in Mitochondrial Amidoxime Reducing Component 1 gene and protection against liver disease. PLoS Genet 17(4): e1009503. https://doi.org/10.1371/journal.pgen.1009503

Published: April 6, 2021

Copyright: © 2021 Emdin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.