Zhang et al reported that SNHG15 can act as a ceRNA to regulate miRNA‐mRNA axis in prostate cancer.30 This study indicated the miR‐338‐3p silencing through SNHG15, which holds binding elements for miR‐338‐3p at its 3′‐UTR, leading to ectopic expression of FKBP1A.30 The overexpression of miR‐338‐3p can significantly decrease the luciferase activity of the wild‐type FKBP1A, but exhibit no influence on the mutant type FKBP1A.30 In summary, SNHG15 elevated FKBP1A expression by sponging miR‐338‐3p at post‐transcriptional level, thus regulating the biological processes of prostate cancer. This evidence concerns the gene FKBP1A and Familial prostate cancer.