Our results clearly indicate that administration of PS-L to Mab infected macrophages significantly enhances their antimicrobial activity leading to intracellular mycobacterial killing, irrespective of CFTR functionality, further supporting and extending the therapeutic value of PS-L, previously reported in the context of MTB/HIV infection, also in the context of the infection with the fast growing, difficult-to-treat, Mab. The gene discussed is CFTR; the disease is infection.