The study of Liang et al. showed that the T66I substitution emerged from a wild-type virus but also from a R263K mutant and from a E138K-R263K double-mutant virus under RAL or EVG pressure . The aim of this study was to assess the effects of the T66I and E138K substitutions, alone and in combination with R263K, on viral replicative capacity and resistance to INI. They showed that the addition of R263K to the T66I substitution did not significantly compromise susceptibility to DTG, while decreasing both viral replicative capacity and strand-transfer activity . The addition of the E138K substitution to the T66I-R263K double-mutant partially compensated for these deficits and resulted in a high level of resistance against EVG but not against DTG or RAL .