In line with this finding, Havcr2 haploinsufficiency primarily enhanced macrophage M1 polarization in 2-week MCD-fed mice, which is consistent with previous study that the increased TIM3 protects MCD-fed mice from liver injury at the early stage [9], but Havcr2 knockdown attenuated macrophage M2 polarization in 5-week MCD-fed mice in vivo, leading to blocking liver NASH fibrosis. This evidence concerns the gene HAVCR2 and digestive system neoplasm.