The subsequent drug–gene interaction networks showed that cinnarizine could participate in the targeted therapy of SRP14 in AML by regulating hyperpolarization-activated cyclic nucleotide gated potassium channel 1 (HCN1), potassium voltage-gated channel subfamily H member 6 (KCNH6), and solute carrier family 6 member 2 (SLC6A2), all of which genes were differentially expressed between the two SRP14 expression phenotypes. This evidence concerns the gene SRP14 and acute myeloid leukemia.