Figure 7. The difference in clinical characteristics between RIPK2 high- and low- expression samples. (A) Distribution of M0 and MX samples among different RIPK2 expression subtypes of KIRC from the TCGA patient cohort and functional modules activation analysis by IPA based on up-regulated genes in RIPK2-high samples. (B) Distribution of tumor stages among different RIPK2 expression subtypes. (C) The distribution plot of the patient’s somatic mutation count (left) and the patient’s fraction of copy number altered (right) among KIRC patients between RIPK2 high- and low- expression samples.