a, Percentage of patients with HCC with mutations in p38γ, CDK1 and CDK2 and the number of HCC mutations in p38γ, CDK1 and CDK2. Data were obtained from the International Cancer Genome Consortium (data from 17 July 2017). b, Expression of p38γ in human primary hepatocytes and in human HCC cell lines (Huh7, HepG2, Snu449 and Snu398) and another type of cancer cells (HTB77). c, Immunoblot analysis of phospho-p38γ and total p38γ in liver extracts from mice lacking IKKγ in the liver (LIKKγKO) and control littermates (WT; left) and from c-Myc transgenic mice (cMYCtg) and wild-type counterparts (right). p38γ phosphorylation was detected only in mice lacking IKKγ specifically in the liver or overexpressing c-Myc. Vinculin served as a loading control. In the western blots each lane corresponds to a different mouse and is representative of at least three independent experiments. d, Immunohistochemical staining of p38γ in human liver with HCC. Negative control, p38γ knockout mice; positive control, p38γ knockout mice infected with human AAVp38γ. The chart shows stratification of p38γ expression in human liver samples as no expression, low, medium, and high expression (n = 46 patients with HCC and n = 11 healthy patients).