To improve livestock and aquaculture-raised fish as food, targeted mutagenesis using genome editing technologies is becoming more realizable. Myostatin (Mstn), which functions as the negative regulator of skeletal muscle growth, is one of the major targets to improve the edible ratio of livestock and farmed fish. We previously reported that the deficiency of Pm-mstn, one of Myostatin paralogs, improves muscle growth and changes body shape in a finfish species, red seabream (Pagrus major), as a result of editing the gene by means of CRISPR/Cas9. In this study, we established Pm-mstnb-deficient red seabream, which is a null-allelic mutant of another paralogous gene of Myostatin in the species, and analyzed their phenotype in terms of growth traits and body shape. A comparison of all growth traits between Pm-mstnbwt/wt and Pm-mstnb-5/-5 revealed no significant differences. In addition, all metrics for body shape, defined as the ratios of body depth, body width, and depth of the caudal peduncle to body length, respectively, were also similar in Pm-mstnbwt/wt and Pm-mstnb-5/-5. Therefore, we concluded that Pm-mstnb does not function as a negative regulator of skeletal muscle growth in red seabream.