Inherited antibiotic resistance has not only been a great career opportunity for many academic and medical scientists, it is an increasingly important clinical problem; people are remaining ill longer and dying of bacterial infections that, in the absence of resistance, would have been cured by antibiotics. Inherited resistance, however, is not the only reason antibiotic treatment fails and for some infections may not be the major reason, at least not yet. For physiological, growth conditions and other reasons, in flasks and even more so in infected animals, bacteria can be refractory to antibiotics to which they are genetically susceptible. In the first part of Dr. Levin's presentation (the first feature), he will review some ancient (1940s and 1950s) and more recent work on this "non-inherited resistance" and its implications for antibiotic treatment with, of course, a non-random sampling of his own in vitro, "in mouse-o," and in silico studies on this subject. Part 2 of Dr. Levin's presentation will be devoted to a serendipitous observation and collaboration; a study of an antagonistic relationship in bacteria. In the course of experiments with populations of E. coli K12 carrying a mutator gene he has observed the evolution of bacteria that inhibited the replication and possibly kills the cells from whence they evolved, their ancestors. This inhibition does not occur until after the onset of stationary phase, is frequency- and density- dependent and requires physical contact between the ancestral and evolved cells, i.e., is contact-dependent inhibition (CDI). Dr. Levin will consider the genetic basis of the evolved CDI and its occurrence without additional evolution in other strains of E. coli. He will conclude with an attempt to tie together the first and second features of this production.