In the current work, we only consider resistance to a single drug, or more precisely, to treatments with a drug or drug combination to which resistance can be generated by the accumulative acquisition of a set of point mutations .

Denote by i the genotype of a cancer cell if it has acquired 1' point mutations (i = 0, 1).

We assume that one point mutation is sufficient to confer high levels of resistance to the maximum possible concentration of drugs administered during therapy.

We denote the genotypes of cells by the number of acquired point mutations : the wild type ‘0’ and the resistant type ‘1’ (see Materials & Methods for a detailed description of the model).

Later on, we will extend this simple model to more realistic cases with multiple cell types and with multiple compartments, where multiple point mutations can successively accrue to confer resistance to exceedingly high drug concentrations [54].

This observation, combined with evidence from our MD simulations that BsFtsZ pocket scores are on par with the scores of point mutations that confer PC190723 resistance in S. aureus (Fig.

Single point mutations were introduced into the S. aureus crystal structure with the mutate residue VMD modeling extension [37].

Furthermore, single point mutations conferring resistance to PC190723 in S. aureus were identified within ftsZ, suggesting that PC190723 specifically binds to S. aureus FtsZ (SaFtsZ).