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Resistance to a given antibiotic ('drug resistance'} is said to be constitutive (= intrinsic ) in cells which lack the specific target site(s) of the antibiotic and/or which are inherently impermeable to the antibiotic. A cell may acquire heritable resistance to antibiotic(s) in several ways. For example, the target site of a given antibiotic may be modified as a result of a chromosomal mutation, so that it functions more or less normally in the presence of otherwise inhibitory concentrations of that antibiotic (see e.g. streptomycin). A single mutant (resistant) cell in a population of susceptible cells can therefore grow and give rise to a population of resistant cells in the presence of the given antibiotic; in bacteria, chromosomal gene(s) specifying antibiotic resistance may be transferred to antibiotic-sensitive cells by conjugation, transduction or transformation. Resistance due to a single mutation is commonly effective against only one type of antibiotic - or against those antibiotics which share the target site. Alternatively, resistance to antibiotic(s) may result from the acquisition of an R plasmid); the acquisition of such a genetic element may confer on a cell resistance to a single antibiotic (and often to related antibiotics) or resistance to two or more unrelated antibiotics; modification of the target site (e.g. MLS antibiotics); an antibiotic-effluxing system (e.g. tetracyclines); or acquisition of an antibiotic-insensitive target enzyme (e.g. folic acid antagonist). If a metabolic pathway is blocked by antibiotic activity, a cell may become insensitive to that antibiotic if it receives a supply of products of the blocked pathway.