The authors analyze the reasons of trivial effectiveness of mineralocorticoid receptor antagonist spironolactone in treating patients with heart failure with moderately reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF), as demonstrated in the TOPCAT (Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist) study. The main reason is said to be steroid base of spironolactone preventing complete blocking of inflammatory and fibrotic processes in heart tissues caused by stimulation of mineralocorticoid receptors (MCRs) by aldosterone. Solution to this problem was creation of non-steroidal molecule AMKR (finerenone) with powerful conformational effect on the receptor preventing it from transcribing the mRNA responsible for release of pro-inflammatory and fibrotic proteins. Preclinical and early clinical trials confirmed preventive and therapeutic effects of finerenone in patients with kidney impairment due to type 2 diabetes mellitus. Along with slowing kidney damage, there was lower risk of cardiovascular complications, particularly heart failure (HF). The only multiple-center placebo-controlled study of finerenone in heart failure (FINEARTS HF) revealed that finerenone significantly reduced the risk of primary composite endpoint defined as cardiovascular mortality or events associated with HF deterioration. Achievements of primary composite endpoint were consistent across all prespecified clinical and demographic subgroups with low risk of side effects, including hyperkalemia. A series of post hoc analyses showed that efficacy of finerenone is independent of gender, age, HF class and baseline LVEF (at least within 40—70%), as well as N-terminal pro-brain natriuretic peptide. The benefits of non-steroidal finerenone were more significant when it was prescribed earlier, and these benefits disappeared within a month after discontinuation of intake. The drug reduced the risk of atrial fibrillation and the need to escalate diuretic therapy. Mean survival of patients with HFpEF/HFmrEF treated with finerenone increased by 3.1 years (p = 0.007), regardless of concomitant therapy with sodium-glucose co-transporter type 2 inhibitors. Currently, finerenone is only approved for patients with type 2 diabetes and chronic kidney disease. However, there is no doubt that finerenone’s position as a pathogenetically justified treatment of HFpEF/HFmrEF corresponds to the highest level and class of evidence, and its inclusion in new guidelines for the treatment of HF is only a matter of time.