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The waxy outer layer of Mycobacterium tuberculosis is rich in mycolic acids, so the inhibitor described is one that blocks mycolic acid synthesis. Isoniazid is activated inside the bacterium and specifically disrupts the fatty-acid synthesis pathway (FAS-II) that builds mycolic acids, preventing the formation of that waxy coat. Without sufficient mycolic acids, the cell wall loses its characteristic waxiness and the bacteria become more susceptible. Rifampin targets RNA polymerase, affecting transcription; Ethambutol disrupts arabinogalactan synthesis in the wall but not the mycolic acid layer itself. A vague label like “Mycolic Acid Inhibitor” isn’t a standard drug name, so the agent that truly achieves inhibiting the waxy wall is isoniazid.