However, its inhibitory effect in the control group was less pronounced, this discrepancy may stem from intrinsic differences in tumor growth rates—slower-growing control tumors may have limited the extent of further inhibition, whereas PPP2CA-knockout tumors, characterized by ITGA5 overexpression and lactate accumulation, likely created a microenvironment more responsive to Triptolide. The gene discussed is ITGA5; the disease is neoplasm.