HAL and glioblastoma: For emerging amino acids, parallel opportunities exist: plasma histidine depletion or high expression of histidine ammonia-lyase (HAL) may predict response to histidine–isoleucine supplementation; YRDC catalytic activity or elevated tRNA modification signatures could identify threonine-dependent glioblastomas; lysine-crotonylation signatures or GCDH overexpression may stratify patients for lysine restriction; and transporter expression, such as SNAT2 for alanine or LAT1 for histidine/isoleucine/threonine, could provide functional markers of dependency.