Like ANKRD52, which is mutated in 4.8% colorectal adenocarcinoma and 1.5% of all cancer types (Fig. 5f), PPP6C harbors recurrent and potentially driver mutations, such as the R264C mutation in 3% melanoma, which may disrupt PPP6C binding to ANKRD52 and thus the enzymatic activity28. This evidence concerns the gene PPP6C and colorectal adenocarcinoma.