Significance Multiple sclerosis (MS) is the most common chronic inflammatory disease of the central nervous system in the western world and leads to devastating disability in young adults, with only limited treatment options currently available. Our recent work demonstrates that pharmacological inhibition of the protein kinase CK2 (CK2) results in inhibition of encephalitogenic human and mouse T helper 17 (T _H 17) cell development and effector function while at the same time promoting development of induced regulatory T (iT _reg ) cells. Hence, modulation of CK2 activity might represent a promising approach for the treatment of MS and other T _H 17 cell-driven inflammatory diseases.