Active cancer is associated with an increased risk of atrial fibrillation (AF), which varies depending on the pre-existing substrate (particularly in older patients), the cancer type and stage, and the anticancer therapeutics being taken. To date, studies have not been able to identify the individual contribution of each factor. During anticancer drug therapy, AF may occur with a frequency of ≈ 15–20% according to several factors, including the patient's baseline cardiovascular toxicity risk and the AF-detection strategies used. Many anticancer drugs have been associated with AF or AF reporting, both in terms of incident and recurrent AF, but robust data are lacking. Only bruton tyrosine kinase inhibitor associated AF (mainly ibrutinib) has a high level of evidence, with a ≈ 3–4-fold higher risk of AF. AF in patients with active cancer is associated with a twofold higher risk of systemic thromboembolism or stroke, and the “TBIP” (Thromboembolic risk, Bleeding risk, drug–drug Interactions, Patient preferences) structured approach must be used to evaluate the need for anticoagulation therapy. AF in patients with active cancer is also associated with a sixfold higher risk of heart failure, and optimal symptom control must be targeted, usually with rate-control drugs (beta-blockers), but a rhythm-control strategy may be proposed in patients remaining symptomatic despite optimal rate-control. AF is generally manageable, with the continuation of anticancer drugs (including ibrutinib); interruption of cancer drugs must be avoided whenever possible and weighed against the risk of cancer progression.