Sea3 was placed previously in the SEACAT epistatic group because of its functional redundancy with Sea2 and Sea4 in response to nutrient conditions (Panchaud et al. 2013b). Therefore, although, it was previously established that inhibition of TORC1 signaling results in shortened telomeres via alteration of the levels of Ku (Ungar et al. 2011), the normal telomere length we observed in haploids bearing a SEA2, SEA3 or SEA4 gene deletion (Figure 1B) may have been due to Sea2, Sea3, and Sea4 functioning redundantly to inhibit the Iml1 complex and support TORC1 signaling as they do in response to nutrients (Panchaud et al. 2013b).