They found that LMS has low somatic mutation burdens (limited to TP53, ATRX, and RB1), depletion of some critical tumour suppressor genes (such as TP53, RB1, CDH1 and PTEN) and high expression of genes linked to myogenic differentiation (such as MYLK, MYH11, ACTG2, miR‐143 and miR‐145) and PI3K‐AKT‐MTOR signalling (typically IGF1R, AKT, RICTOR and MTOR).1, 2. This evidence concerns the gene AKT1 and neoplasm.