In fact, Hou et al. [64] reported that sFgl2 activates the ERK1/2-STAT3 pathway by activating SHP2, thereby biasing macrophages toward a pro-repair phenotype, which is associated with endometriosis progression, and our study also revealed that the level of p-SHP2 increased in the presence of sFgl2, and the level of p-SHP2 was the highest in the sFgl2-MSC treatment group because MSCs induced the expression of CD32b in CD4+ T cells; the level of p-SHP2 decreased after blocking CD32b. The gene discussed is CD4; the disease is endometriosis.