This phenomenon of acquired drug resistance occurs not only with M tuberculosis but also with M kansasii for rifamycins (rpoβ gene mutation), M avium complex with macrolides (23S ribosomal RNA gene mutation), and “M abscessus” with macrolides (23S ribosomal RNA gene mutation).,,,, While an active erm gene is the primary mechanism for in vitro “M abscessus” macrolide resistance, approximately 20% of M abscessus subspecies abscessus isolates have a mutation that inactivates the erm gene, making the isolate macrolide susceptible and significantly easier to treat. Choi et al showed that macrolide-susceptible M abscessus subspecies massiliense isolates with an inactive erm gene are significantly more likely to respond to antimycobacterial therapy including a macrolide than M abscessus subspecies abscessus isolates with an active erm gene. The clear message is that macrolide resistance, for any reason, is a significant impediment to successful therapy for disease caused by any “M abscessus” subspecies. Furthermore, even if an M abscessus subspecies abscessus fortuitously has an inactive erm gene, it is still possible to develop acquired mutational macrolide resistance. The most significant aspect of acquired mutational drug resistance is that it is preventable.