GSK3B and infection: It has also been demonstrated that coxsackievirus B3 infection upregulated GSK3β levels in a mouse model [170] and increased the activity of GSK3β in HeLa cells, resulting in reduced β-catenin amounts, infection-associated cytopathic effects, and apoptosis as well as increased viral progeny release, effects that could be blocked by GSK3 inhibition [171].