The Lac plasmids in two Klebsiella strains, V9A and RE1544, give characteristic Lac-permease defective mutations which produce a lactose-negative (ML−) phenotype in the host strain, in spite of the presence of a lac operon on the chromosome. These ML− clones can revert to the wild-type (ML+) phenotype, and the mechanism of this reversion is examined. In V9A carrying its own Lac plasmid (FKlac), it is shown that reversion of ML− to ML+ is usually the result of mutation to constitutivity of one of two galactoside permeases which are not induced by lactose but accumulate lactose when otherwise induced or made constitutive. However, in one out of the 51 ML+ revertants tested the mechanism of reversion appeared to be a change back to wild type of the Lac plasmid's own permease gene. In V9A carrying the Lac plasmid (pRE6) from RE1544, successive changes of phenotype were obtained of ML+ to ML− to ML+ to ML− to ML+; these were all found to be the result of changes in the plasmid permease gene, and could be simply explained if an IS sequence could insert and excise from this gene.