From what I've seen from failed NASH drugs they try to resolve NASH one of two ways. They either try to reduce the liver fat hoping that will reduce fibrosis or try to reduce inflammation by very specific targeting.

CCR5 blockade by leronlimab can increase production of brown fat (good) cells in preference to white fat (bad) cells. Leronlimab also increases energy efficiency in brown fat leading to a reduction in white fat. White fat also increases CCR5 expression leading to an inflammatory state that leronlimab would reverse. Then of course leronlimab targets multiple other inflammatory pathways.

With leronlimab attacking both fat reduction and inflammation it has a much higher chance of succeeding than previous drugs.