The nontuberculous mycobacteria (NTM) are ubiquitous environmental bacteria found in soil, ground water, and in municipal water supplies. Rates of infections by NTM are increasing with more than 100,000 people in the U.S. diagnosed each year. NTM infections are common in individuals with underlying lung diseases such as cystic fibrosis or COPD, where chronic infections can lead to poor patient outcomes, and there is a clear need for better anti-NTM therapeutic targets as current treatments often require more than one year using a cocktail of antibiotics. Around a decade ago, it was discovered that NTM and other Gram-positive bacteria utilize a heme biosynthesis pathway that generates a coproporphyrin intermediate instead of a protoporphyrin intermediate. The discovery of this pathway, termed the coproporphyrin dependent (CPD) pathway, opened up the possibility of targeting heme biosynthesis in Gram-positive bacteria as the terminal three steps had enzymes and metabolites not found in the canonical protoporphyrin dependent pathway used by humans. However, very little is known about how NTM maintain heme homeostasis or how NTM incorporate exogenous heme into their metabolism. Research in our lab has focused on the effects of exogenous heme on NTM biofilm formation and understanding how NTM regulate heme biosynthesis. We have found that heme and hemoglobin support NTM growth and alter biofilm formation and that exogenous heme is likely used as a nutrient by these bacteria. In addition, exogenous heme reduces NTM porphyrin production and secretion. The role of porphyrin secretion in NTM biology and in heme homeostasis is still under investigation, but it sheds light on the likelihood that heme biosynthesis is regulated at multiple points in the CPD pathway.