Mucoid mutants of Salmonella enterica serovar Typhimurium isolated by resistance to mecillinam include lon (27%) and rcsC (8%) mutants but the most frequent class (65%) is affected in a new gene (mucM) located at centisome 76. mucM cells are shorter than mucM+ cells and rcsB mutations normalize size and response to mecillinam. Expression of ftsA1p, the ftsA-ftsZ promoter submitted to RcsB stimulation, is greatly increased in mucM mutants, and this expression is dependent on RcsB and ftsA1p. It is proposed that the mucM product interferes with RcsB activation. Mucoidy results from the activation of cps genes and mecillinam resistance from ftsA-ftsZ overexpression, both traits caused by the increased activity of the RcsB effector. The same mechanism seems to be responsible for the resistance of mucoid rcsC mutants to mecillinam but the resistance of lon mutants is not dependent on RcsB and so responds to a different cause.