Consequently, the vast majority of recurrent mutations predominantly result in loss-of-function of tumor suppressors (Figure 2), including BAP1, TP53, NF2, SETD2, LATS2, DDX3X, and ULK2, as well as copy number losses in BAP1, TP53, CDKN2A/B, NF2, LATS2, LATS1 and gains in RPTOR and BRD4 as well as other genomic alterations (Bueno et al., 2016; Hmeljak et al., 2018). Here, LATS2 is linked to neoplasm.