Abstract
Studies of somatic mutations have historically focused on those occurring during carcinogenesis, but recent research suggests functional mutations can accumulate in the absence of cancer. Zhu and colleagues recently published an extensive analysis of exome sequencing from 82 livers, describing a complex mutational landscape and identifying mutations that promote cellular fitness without inducing carcinogenesis (1). Advancing fibrosis stage was associated with increasing number and size of mutant clones which included recurrent mutations in genes PKD1, PPARGC1B, KMT2D, and ARID1A.
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