17 Single-pulse transcranial magnetic stimulation (TMS) elicits an evoked 18 electroencephalography (EEG) potential (TMS-evoked potential, TEP), which is interpreted 19 as direct evidence of cortical reactivity to TMS. Thus, combining TMS with EEG may enable 20 the mechanistic investigation of how TMS treatment paradigms engage network targets in 21 the brain. However, there remains a central controversy about whether the TEP is a genuine 22 marker of cortical reactivity to TMS or the TEP is contaminated by responses to peripheral 23 somatosensory and auditory inputs. Resolving this controversy is of great significance for 24 the field and will validate TMS as a tool to probe networks of interest in cognitive and clinical 25 neuroscience. Here, we delineated the TEP's cortical origins by localizing successive TEP 26 components in time and space and modulating them subsequently with transcranial direct 27 current stimulation (tDCS). We collected both motor evoked potentials (MEPs) and TEPs 28 elicited by suprathreshold single-pulse TMS to the left primary motor cortex (M1). We found 29 that the earliest TEP component (P25) was localized on the TMS target location (left M1) 30 and the following TEP components (N45 and P60) largely were localized on the primary 31 somatosensory cortex, which may reflect afferent input by hand-muscle twitches. The later 32 TEP components (N100, P180, and N280) largely were localized to the auditory cortex. To 33 casually test that these components reflect cortical and corticospinal excitability, we applied 34 tDCS to the left M1. As hypothesized, we found that tDCS modulated cortical and 35 corticospinal excitability selectively by modulating the pre-stimulus mu-rhythm oscillatory 36 power. Together, our findings provide causal evidence that the early TEP components 37 reflect cortical reactivity to TMS. 38 39 tDCS 3 41 Introduction 42 Combined transcranial magnetic stimulation (TMS) and electroencephalography (EEG) 43 provide an opportunity to quantify brain network dynamics by pinging them with TMS[1]. The 44 TMS-evoked potential (TEP), which is considered a reflection of cortical reactivity to TMS, 45 has been shown to have diagnostic value in a variety of neurological and psychiatric 46 disorders[2]. However, there is ongoing controversy about the origin of the TEP. A recent 47 study claimed that the stimulation of peripheral nerves and the TMS coil's loud clicking 48 sound may confound the TEP amplitude[3]. Specifically, sham TMS elicited EEG potentials 49 that were correlated highly with those by real TMS, despite the use of sophisticated 50 procedures to attenuate the somatosensory and auditory confounds. In rebuttal of this 51 publication, it was suggested that insufficient TMS intensity and incomplete auditory 52 masking may explain the sensory-dominant evoked potentials in the experiment[4]. 53 Nonetheless, residual auditory input is unavoidable in TMS studies[5] because of air and 54 bone conduction from the TMS clicking sound[6,7]. Thus, it continues to be debated whether...