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Following damage to the primary visual cortex, some patients exhibit “blindsight,” where they report a loss of awareness while retaining the ability to discriminate visual stimuli above chance. Transient disruption of occipital regions with TMS can produce a similar dissociation, known as TMS-induced blindsight. The neural basis of this residual vision is controversial, with some studies attributing it to the retinotectal pathway via the superior colliculus whereas others implicate spared projections that originate predominantly from the LGN. Here we contrasted these accounts by combining TMS with visual stimuli that either activate or bypass the retinotectal and magnocellular (R/M) pathways. We found that the residual capacity of TMS-induced blindsight occurs for stimuli that bypass the R/M pathways, indicating that such pathways, which include those to the superior colliculus, are not critical. We also found that the …