Correction: Zhang et al. Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B₁-Induced Oxidative Damage. Antioxidants 2022, 11, 1787

In the original publication [1], a mistake was identified in Figure 4 as published. The explanation in Figure 4E is wrong. The corrected Figure 4 appears below. The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.

Figure 4.

Treatment with inhibitor M2 leads to the highest resistance to aflatoxin B₁ in vitro. (A) Workflow of the structure-based virtual screening to identify inhibitors targeting BACH1. (B) Validation of the top three inhibitors (M1, M2, and M3) in Huh7 cells by CCK-8 assays. (C) Comparation of Huh7 tolerance to different AFB₁ concentrations with and without M2 treatment. (D) The relative fluorescence intensity of AFB₁-DNA adducts in Huh7 cells with and without M2 treatment. (E) Representative light microscopy images of AFB₁-treated PK-15 cells with or without M2 treatment. Scale bar, 100 μm. (F) The IC₅₀ assays for AFB₁ in PK-15 cells with and without M2 treatment determined with CCK-8 assays. (G) The relative fluorescence intensity of AFB₁-DNA adducts in PK-15 cells with and without M2 treatment. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, not significant. p values were determined with two-tailed Student’s t-tests. AFB₁, aflatoxin B₁; M1, 1-Piperazineethanol, 4-phenyl-α-[[(3,4,5-trimethoxyphenyl)methoxy]methyl]; M2, 1-Piperazineethanol,α-[(1,3-benzodioxol-5-yloxy)methyl]-4-(2-methoxyphenyl); M3, 1,2-Ethanediamine, N1, N1, N2, N2-tetrakis (1H-benzimidazol-2-ylmethyl).