Conversely, Beuselinck et al. performed a multi-omics analysis and identified four molecular tumor subtypes able to predict clinical outcome and response to sunitinib in metastatic ccRCC: ccrcc1 (“c-myc-up”) and ccrcc4 (“c-myc-up and immune-up”) characterized by the upregulation of MYC targets and shorter PFS, OS and poorer response to sunitinib; ccrcc2 (“classical”) and ccrcc3 (“normal-like”) with a higher expression of the pro-angiogenic HIF-VEGF-VEGFR-pathway, longer OS and better TKI response. Here, MYC is linked to neoplasm.