Increased FC is often conceived as compensatory reallocation or dedifferentiation.[23,38–41] Inflammation may modulate the compensatory process.[42] In the early course of SD, proinflammatory cytokines (i.e., tumor necrosis factor and interleukin-6) activate the astrocytes and show hyperfunction (increased blood flow and metabolism).[43] Regional hyperfunction can contribute to the increased FC and activity in this region. Here, TNF is linked to Salla disease.