The symptoms of secondary hyperparathyroidism (SHPT) were substantially changed by the availability of cinacalcet (CC). The recent ADVANCE study, which was a prospective randomized trial comparing two treatment strategies—CC plus low doses of calcitriol analogues (CA) versus higher doses of CA without CC—reports the absence of difference in the primary endpoint, i.e. coronary artery calcification score progression after 12months. The progression of coronary calcification was related to the initial hypercalcemia and hyperphosphataemia, and low serum PTH level. What was the rationale for defining SHPT with only serum PTH value of more than 300pg/mL or more than 150pg/mL associated with a high Ca×P product? Why was this coronary score chosen as the primary endpoint and why was a seemingly short observational period used? Is it correct to consider all forms of SHPT equivalent in terms of set point, response to conventional treatment, or vascular and bone consequences? Why are the biological values of patients not provided? Were the CAs, dialysate calcium, and PTH assay values really equal? Why were only calcium-based phosphate binders used? The main controversial point of the study was to consider all HPT cases as equivalent and able to be treated by one fixed strategy. Therefore, the nephrologist community should conduct relevant independent studies in order to improve the diagnosis and treatment of SHPT.