Like BTKi-related AF, the inhibition of the Phosphoinositide 3-kinase (PI3K) pathway may play a role in cellular remodeling mechanisms, potentially leading to vascular tissue fibrosis; however, the cause of hypertension observed in BTKi treatment remains uncertain, as it is unclear whether it results from off-target kinase inhibition or systemic inflammatory changes that increase the risk of hypertension development [58]. The gene discussed is IBTK; the disease is atrial fibrillation.