Recent work by our group showed that cold-induced vasodilation (CIVD) is a centrally originating phenomenon caused by sympathetic vasoconstrictor withdrawal; it is dependent on excess heat, and it may be triggered by excess heat with the purpose of preserving thermal balance (Flouris et al. 2008; Flouris and Cheung 2009a, b). To this effect, Daanen and Layden (2009) recently argued that, instead, our data show that CIVD is of peripheral origin. Thus, our aim in this letter is to briefly clarify misconceptions that may have led Daanen and Layden to questionable inferences. We have reported a sympathetic withdrawal during CIVD (Flouris and Cheung 2009b) in line with the evidence that CIVD is attributed to an interruption of adrenergic neurotransmission (Johnson et al. 1986). Given that sympathetic activity is generally inversely associated with core temperature (Sawasaki et al. 2001), Daanen and Layden derived that ‘‘...the sympathetic activity must have been continuously increasing during the cooling period’’ which led them to the conclusion that CIVD in our study ‘‘...was of peripheral rather than central origin’’. Since our experiment demonstrated a sympathetic withdrawal—not activation—during CIVD, the logic and conclusion of Daanen and Layden are fallacious. In their letter, Daanen and Layden argue that careful reading of the literature does not support our claim that CIVD can be induced by whole body cold exposure. Indeed, Montgomery and Williams (1977) did not investigate CIVD and we were misled by their reference to ‘‘cold vasodilation’’ in their discussion. However, the remaining claims of Daanen and Layden are inaccurate as Berry et al. studied CIVD [‘‘...the occurrence of cold-induced vasodilation (CIVD) found in the present study agrees with that observed by...’’ (1984)], while Steegmann [‘‘...90 min of exposure to 1 C air moving over the face and body at about 6 m/min’’ (1979)] as well as Brajkovic and Ducharme [‘‘...subjects walked comfortably (4.8 km/h) on a treadmill during exposure to four 90-min tests, each at a different environmental condition...’’ (2006)] did, in fact, expose the entire body to cold, not just the face. Moreover, Shitzer’s group did induce CIVD via whole body cold exposure in the papers that we referenced (Shitzer 1998; Shitzer et al. 1991, 1998a, b). There is, obviously, a mistake here as Daanen and Layden refer to papers by Shitzer’s group (Shitzer et al. 1996, 1997) that we never referenced. A final point of Daanen and Layden was that the phenomenon we interpreted as CIVD in our original experiment (Flouris et al. 2008) was a normal heat loss mechanism because, at times, finger temperature was up to 33.5 C. However, finger temperature for a large part of the experiment was below 15 C and was very often as low as 5 C, confirming that the cold stimulus to the hands was strong enough to evoke CIVD. Also, similar insulation of the body and hands has been used in several studies in the past (Santee et al. 1990; Shitzer 1998; Shitzer et al. 1991, 1998a, b), all of which incorporated shorter and less severe exposures compared to ours but reported a large number of CIVDs. In conclusion, no salient data or arguments have thus far been presented refuting that CIVD is a centrally originating Communicated by Susan Ward.