To determine if overexpressed mutant tau caused HSF1 protein loss and eIF2α-CHOP activation in vitro, we transiently transfected N2a neuroblastoma cells with wild-type- or P301L- or ΔK280-TauRD. Tau protein typically does not form amyloid fibrils in vitro because of its intrinsic hydrophilic feature. The gene discussed is DDIT3; the disease is neuroblastoma.