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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 is 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 We do show in this study, however,  that DmCa\textsubscript{v}2, DmCa\textsubscript{v}3-null mutants sleep more than controls.  We have been unable so far to assign this phenotype to  a member of the high voltage-activated (HVA) Ca\textsubscript{v}2 subfamily of Ca\textsuperscript{2+} channels, may specific neuronal subpopulation, but our results suggest an overall wake-promoting role for DmCa\textsubscript{v}3.  This wake-promoting function  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 seems to  be compensating for the loss independent  ofDmCa\textsubscript{v}3 in  the circadian clock, as  DmCa\textsubscript{v}3-null mutants.  Flies lacking DmCa\textsubscript{v}3 do, however, mutants  show a clear sleep phenotype, suggesting that if such compensation is occurring, it is inadequate weak but significant rhythmicity  in the circuits that regulate sleep/wake behavior. \textcolor{red}{Do we really need this caveat on HVA channels compensating for the loss constant darkness and normal oscillation  of the LVA channel? I am not sure it fits in this narrative.} core clock gene \emph{period}.  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 Judging from  the core clock gene \emph{period}.  This wake-promoting function and lack complexity  of deep sleep T-type physiology so far reported  in invertebrate seems to mice, it will  be relevant for surveillance against predation.  Invertebrates may lack deep sleep state such as non-rapid eye sleep (NREM) because they lack the sleep-promoting mechanism that depends on T-type Ca\textsuperscript{2+} channel.  This species-dependent differences of sleep regulation may give insights interesting to see whether future studies focused  on the evolution technically demanding study  of sleep pattern differentiation isoform-specific expression patterns  and the mechanism. isoform-specific rescues in both mice and flies will clarify how T-type channels can at various times both enhance and reduce sleep.