The recent discoveries of somatic mutations in RP genes in hematological cancers (such as T-cell acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL) and multiple myeloma) and solid tumors (such as breast cancer and melanoma) emphasize that defects in ribosome biogenesis could potentially promote oncogenic transformation.23 In fact, deletions in RP genes are common events across human cancers, particularly in concert with TP53 mutations. This evidence concerns the gene BLOC1S3 and melanoma.