Kinesin and dynein are two types of ATP-dependent mechanochemical motors that are involved in the transport of a variety of cytoplasmic cargos along microtubule fibers, the regulation of microtubule stability and the maintenance of centrosome integrity. Besides being responsible for both the maintenance of cell morphology and physiological functions, kinesins also play important roles in cell division, cell motility, spindle assembly, chromosome aggregation and separation. Although its role might be different in different types of cancer, some KIFS have been known to play a role in many types of cancer development, and they have also been pointed as interacting with viruses during viral infection, notably during viral egress. With an ongoing need for novel anti-retroviral treatments, these findings open the way for further studies with this motor protein, aiming the development of new and more efficient treatment strategies for chronic diseases such as AIDS caused by these fast-mutating viruses. This article presents an overview of KIF4 structure and functions and focus on its interactions with the Gag retroviral polyprotein during retroviral infection. Moreover, we draw attention to KIFs clinical potential as a therapeutic target to block retroviral infections by interfering with the production of new viral particles through microtubules destabilization.