To identify clinically used anticancer drugs whose effects are influenced by CYP2D6 activity, we established cancer cell models proficient or deficient in CYP2D6 activity by introducing the wild-type CYP2D6∗1 and LoF CYP2D6∗4 variant containing the splice site substitution G1846A (rs3892097), which creates a new acceptor site one base downstream of exon 4. This evidence concerns the gene CYP2D6 and cancer.