MYLK and hyperlipidemia: Combined with our findings, we hypothesize that hyperlipidemia can increase the level of DCA in the blood, which leads to the disturbance of the distribution of TJPs among the endothelial cells of the AVP through the MLCK-P-MLC2 pathway, which may be accompanied by a decrease in the expression of TJPs, leading to VEBF injury of the hemorrhoidal AVP and thus contributing to the development of hemorrhoids.