Cyclin‐dependent kinases (CDKs), together with their cyclin partners, are the master cell cycle regulators. Remarkably, the cyclin family was extended to include atypical cyclins, characterized by distinctive structural features, but their partner CDKs remain elusive. Here, we conducted a yeast two‐hybrid screen to identify new atypical cyclin–CDK complexes. We identified 10 new complexes, including a complex between CDK6 and cyclin I (CCNI), which was found to be active against retinoblastoma protein.CCNIupregulation increased the proliferation of breast cancer cellsin vitroandin vivo, with a magnitude similar to that seen upon cyclin D upregulation, an effect that was abrogated byCDK6silencing or palbociclib treatment. In line with these findings,CCNIdownregulation led to a decrease in cell number and a reduction in the percentage of cells reaching S phase. Finally,CCNIupregulation correlated with the high expression of E2F target genes in large panels of cancer cell lines and tissue samples from breast cancer patients. In conclusion, we unveil CCNI as a new player in the pathways that activate CDK6, enriching the wiring of cell cycle control.