In different SSPE cases, mutations either impair the expression and particle assembly organizing function of the M protein (23, –, 27) or reduce the F protein stability and favor its receptor-independent activation, or truncate the F protein cytoplasmic tail, uncoupling the fusion inhibitory function exerted by the M protein (28, –, 33). The gene discussed is MYOM2; the disease is subacute sclerosing panencephalitis.