(A) In situ hybridization of cia-MAF in HCC tissue microarray containing 90 peri-tumor, 58 stage 1, 29 stage 2, and 3 stage 3 tumor tissues. Typical images are in the left panels and calculated intensities are in the right panel. Scale bars: 30 μm. The details of HCC tissue microarray are listed in Supplemental Table 4. (B) Violin plot showing cia-MAF intensities in HCC samples with (+) or without (–) relapse. Individual samples, medium levels, minimum, maximum, and quarter levels are shown. (C) Kaplan–Meier survival analysis of cia-MAF^hi and cia-MAF^lo samples, which are grouped according to the average cia-MAF expression level. (D) Percentage distribution of CD44⁺ TICs in cia-MAF^lo (left) and cia-MAF^hi (right) samples. (E) Coexpression of cia-MAF and liver TIC marker CD44 in 90 liver cancer tissues. (F) Northern blot of cia-MAF in CD44⁺ TICs (C) and CD44^– non-TICs (N). 18S rRNA served as a loading control. Typical images are in the left panel and signal intensities are quantified with Image J (right). (G) FISH of cia-MAF in spheres and nonspheres, which were derived from primary HCC cells. Scale bars: 20 μm. (H) FISH of cia-Maf in clone #2 and clone #6, which were derived from YFP⁺ mouse liver cancer cells. Scale bars: 20 μm. *P < 0.05, **P < 0.05, ***P < 0.001. Significance was determined by 1-tailed Student’s t test (A, B, and F), log-rank test (C), and χ² test (D). For all representative images, n = 3 independent experiments performed with similar results.