In this research, we studied the individual and combined effects of arsenic and vanadium on the cerebellum ofmice. Mice were subjected to arsenic and vanadium individually and in combination for 21 days. Twenty-four hours after thelast administration, the mice were subjected to open field and rotarod tests after which the cerebellar tissues were harvestedfor biochemical analysis of the levels of malondialdehyde (MDA), catalase (CAT), caspase-3, tumor necrosis factor alpha(TNF-α), nuclear factor erythroid 2-related factor 2 (Nrf2), interleukin-1 beta (IL-1β), dopamine, serotonin, acetylcholine, andacetylcholinesterase. The hematoxylin and eosin stain was employed to explore histopathological event in the cerebellar tissue. Themice were either subjected to arsenic or vanadium or their combination showed significant short fall respectively in the open fieldand rotarod tests. There was an aggravated shortfall in the mice exposed to arsenic+vanadium combination. Furthermore, our datashowed that exposure to the combination of arsenic and vanadium provoked synergistic neurotoxicity in the cerebellum of the micesubjected to arsenic+vanadium resulting into disturbance of locomotor and the production of neurodegenerative characteristicsin the cerebellum. Relative to the control group, the levels of MDA, CAT, caspase-3, TNF-α, Nrf2, IL-1β, dopamine, serotonin,acetylcholine, and acetylcholinesterase were adversely modulated in the arsenic-treated, vanadium-treated and in the group exposedto the combination of arsenic+vanadium. The histopathology of the cerebellum showed that exposure to arsenic, vanadium, andtheir combination produced neurodegenerative effects. The study conclude that exposure to arsenic and vanadium, as well as theircombination, had a considerable influence on cerebellar tissue, culminating in a synergistic toxic effect.