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Although Ca\textsubscript{v}3.1 knockout mice lack the slow wave oscillations characteristic of deep sleep and show reduced total sleep\cite{Lee:2004ey}, when the knockout is limited to the rostral midline thalamus, sleep is still reduced, but delta waves are mildly increased\cite{anderson:2005aa}. Another more recent study showed that treatment with the T-type-specific channel blocker TTA-A2 enhances sleep and delta rhythms in wild type mice but not Ca\textsubscript{v}3.1/Ca\textsubscript{v}3.3 double knockout mice\cite{kraus:2010aa}. In other words, manipulation of T-type channels can both enhance and reduce total sleep and deep delta-wave sleep depending on the experimental context.  Although perhaps disrespectful of the actual complexity of the situation, the subtle phenotypes of the homozygous viable Ca\textsubscript{v}3 mutant mice are often ascribed to functional compensation among the various Ca\textsubscript{v}3.1-3 isoforms. \textcolor{red}{Maybe a citation here?}  It isperhaps  surprising, then, that despite its broad and relatively strong expression across adult fly brains, null mutants of the one and only fly T-type channel, DmCa\textsubscript{v}3, are also homozygous viable and lack any overt phenotypes. One previous study suggested that DmCa\textsubscript{v}2, a member of the high voltage-activated (HVA) Ca\textsubscript{v}2 subfamily of Ca\textsuperscript{2+} channels, may also somehow participate in the generation of low voltage-activated (LVA) Ca\textsuperscript{2+} currents\cite{Ryglewski:2012jk}.  It is, therefore, plausible that other HVA channels could be compensating for the loss of DmCa\textsubscript{v}3 in the DmCa\textsubscript{v}3-null mutants. Flies lacking DmCa\textsubscript{v}3 do, however, show a clear sleep phenotype, suggesting that if such compensation is occurring, it is inadequate in the circuits that regulate sleep/wake behavior. \textcolor{red}{Do we really need this caveat on HVA channels compensating for the loss of the LVA channel? I am not sure it fits in this narrative.}  In this study, we show that DmCa\textsubscript{v}3-null mutants sleep more than controls, suggesting an overall wake-promoting role for DmCa\textsubscript{v}3.  This wake-promoting function seems to be independent of the circadian clock, as DmCa\textsubscript{v}3-null mutants show weak but significant rhythmicity in constant darkness and normal oscillation of the core clock gene \emph{period}.